Biochemical Genetics[JOURNAL]
Sun
200 papers
Dual Inhibition of PI3K-AKT Signaling Pathway by miR-542 Overexpression in Cervical Cancer.
Rahimi-Moghaddam A, Ghorbanmehr N, Gharbi S
Biochem Genet · 2025 Oct · PMID 41082028 · Publisher ↗
The PI3K-AKT signaling pathway (SP) has been introduced as a key regulatory pathway in cervical cancer (CC). Inhibition of this SP could be a therapeutic strategy in CC. Our previous bioinformatics analysis exhibited tha...
The PI3K-AKT signaling pathway (SP) has been introduced as a key regulatory pathway in cervical cancer (CC). Inhibition of this SP could be a therapeutic strategy in CC. Our previous bioinformatics analysis exhibited that miR-542 could have a dual inhibitory function on this SP by targeting PIK3CB and AKT1 genes with its two arms (-3p and -5p) and proposed it as an appropriate therapeutic target for CC. The current study experimentally investigated the dual inhibitory function of miR-542 on the PI3K-AKT SP. qRT-PCR was performed following transfection of the recombinant pEGFP-C1 vector containing miR-542 precursor into the CaSki and miR-542 overexpression to quantify the expression level of target genes of miR-542 (AKT1 and PIK3CB) as regulators of PI3K-AKT SP and their downstream genes affecting cell proliferation and apoptosis (CDKN1A and BCL2). In addition, the effect of overexpression of miR-542 on cell cycle and apoptosis was examined by flow cytometry using propidium iodide and PE Annexin V/7-AAD staining, respectively. The recombinant cells showed a significant decrease in the expression of AKT1, PIK3CB, and BCL2 genes, and a significant increase in the level of CDKN1A gene expression, simultaneously with the highest overexpression of miR-542 at 48 h post-transfection. Furthermore, the apoptosis was remarkably induced and the cell cycle was arrested in recombinant cells compared to mock cells. miR-542 promoted apoptosis and cell cycle arrest by dual inhibiting the PI3K/AKT SP. It may be introduced as an appropriate target for CC treatment.
Association of IL1B Gene Polymorphisms (rs1143634 and rs16944) with Schizophrenia in Iranian Patients.
Mehrabi S, Mirtabatabaei L, Shakerian S … +6 more , Forouzesh F, Razavi M, Tavabe-Ghavami TS, Mohammadi-Lapevandani M, Ghasemi Y, Alizadeh F
Biochem Genet · 2025 Oct · PMID 41082027 · Publisher ↗
Schizophrenia (SCZ) is a deleterious neuropsychological disorder with a worldwide incidence of 1% and unknown etiology. Understanding the role of genetic variants in disease development would enable us to explain the dis...
Schizophrenia (SCZ) is a deleterious neuropsychological disorder with a worldwide incidence of 1% and unknown etiology. Understanding the role of genetic variants in disease development would enable us to explain the disorder's molecular mechanism and find a more effective prognostic approach. Several studies in various European and East Asian populations have displayed the association of schizophrenia with functional polymorphisms such as rs16944 and rs1143634 that lie within inflammatory pathway genes. This study aimed to evaluate the association of Interleukin-1 beta (IL1B) variants (rs16944, rs1143634) with schizophrenia in the Iranian population for the first time. 565 individuals (240 cases and 325 controls) were recruited. Genotyping was conducted for IL1B single nucleotide polymorphisms (SNPs) (rs16944 and rs1143634) using polymerase chain reaction-Restriction fragment length polymorphism (PCR-RFLP). In addition, the haplotype analysis was conducted. All statistical analysis was performed using SPSS version 26. Regarding rs1143634 (C > T), T carrier genotypes (CT, TT) compared to CC homozygous genotypes showed a significantly more protective effect (p-value < 0.001). Similarly, concerning the co-dominant model, CT heterozygous genotypes in comparison with homozygous genotypes (CC, TT) illustrated a protective impact regarding schizophrenia (p-value < 0.001). Findings showed a significant difference between cases and healthy controls regarding the rs1143634 (C > T) allele frequency (p-value = 0.025), whereas it determined no considerable difference given rs16944 (p-value = 0.41). Furthermore, in the case of rs16944 (T > C), we found no significant association between case and control groups (p-value = 0.69). Haplotype analysis demonstrated that the C-C (rs1143634-rs16944) haplotype was significantly associated with the risk of schizophrenia (p-value = 0.013). The findings suggest that IL1B rs1143634 (C > T) is significantly associated with SCZ in the Iranian population.
Retraction Note: Sodium Butyrate Inhibits the Malignant Proliferation of Colon Cancer Cells via the miR-183/DNAJB4 Axis.
Pan D, Hao J, Wu T … +6 more , Shen T, Yu K, Li Q, Hu R, Yang Z, Li Y
Biochem Genet · 2025 Dec · PMID 41060569 · Publisher ↗
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Associations between VMAT1 Polymorphisms and Obesity.
Azizi S, Dadyar M, Eslami S … +3 more , Hussen BM, Sayad A, Ghafouri-Fard S
Biochem Genet · 2025 Oct · PMID 41051620 · Publisher ↗
Obesity is a multifactorial disorder with a significant genetic component. Variants within the VMAT1 gene have been proposed to influence susceptibility to obesity. This study aimed to assess the association of two singl...
Obesity is a multifactorial disorder with a significant genetic component. Variants within the VMAT1 gene have been proposed to influence susceptibility to obesity. This study aimed to assess the association of two single-nucleotide polymorphisms (SNPs), rs2270637 and rs1390938, within VMAT1 with obesity risk in an Iranian population undergoing sleeve gastrectomy. A number of obese patients selected for sleeve gastrectomy were genotyped for rs2270637 and rs1390938. Genotype and allele frequencies were compared using logistic regression under different genetic models (allelic, co-dominant, and recessive). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to assess the strength of associations. The rs1390938 SNP showed a significant association with obesity in the allelic model, with the A allele conferring protection against obesity (OR = 0.70, 95% CI 0.55-0.88, P = 0.003). In the co-dominant model, individuals with the AA genotype had a significantly reduced risk of obesity compared to those with the GG genotype (OR = 0.20, 95% CI 0.092-0.43, P = 0.000058). Similarly, in the recessive model, the AA genotype remained protective (OR = 0.21, 95% CI 0.099-0.46, P = 0.000087). The rs2270637 SNP also showed significant associations with obesity in co-dominant and recessive models. The GG genotype was protective compared to the CC genotype (OR = 0.11, 95% CI 0.034-0.41, P = 0.001) and compared to the combined GC + CC genotypes (OR = 0.11, 95% CI 0.034-0.40, P = 0.001). Both rs1390938 and rs2270637 polymorphisms in the VMAT1 gene are significantly associated with obesity risk in the studied Iranian cohort. The findings support the role of VMAT1 as a potential genetic susceptibility locus for obesity.
m6A Modification-Mediated LINC01547 Promotes Pancreatic Cancer Growth and Gemcitabine Resistance Through miR-34a-5p/MYH9 Axis.
Lu G, Gong J, Chen Y … +3 more , Li X, Wang J, Hu J
Biochem Genet · 2025 Oct · PMID 41046501 · Publisher ↗
Gemcitabine (GEM) resistance undermines chemotherapy efficacy for pancreatic ductal adenocarcinoma (PDAC), resulting in poor prognosis. Long non-coding RNAs (LncRNAs) participate in various malignant tumors, including PD...
Gemcitabine (GEM) resistance undermines chemotherapy efficacy for pancreatic ductal adenocarcinoma (PDAC), resulting in poor prognosis. Long non-coding RNAs (LncRNAs) participate in various malignant tumors, including PDAC. However, their roles in GEM resistance require further elucidation. Here, we investigated the function of LINC01547 in PDAC progression and chemoresistance. LINC01547 was significantly upregulated in PDAC tissues and cell lines, and its high expression correlated with unfavorable patient outcomes. Silencing LINC01547 dramatically suppressed cellular proliferation, sphere formation capability and enhanced GEM sensitivity of PDAC cells both in vitro and in vivo experiments. Mechanistically, LINC01547 as a competing endogenous RNA that could regulate miR-34a-5p. RNA-sequencing and luciferase reporter analysis demonstrated that miR-34a-5p directly targets MYH9. Additionally, METTL3 mediated m6A modification boosted the RNA stabilization and upregulation of LINC01547. Taken together, these findings indicate that LINC01547 could promote tumor progression and gemcitabine resistance in PDAC via miR-34a-5p/MYH9 axis, highlighting LINC01547 as a potential biomarker and therapeutic target for overcoming chemoresistance in PDAC.
Long Noncoding RNA H19 Overexpression Inhibits High Glucose-Induced Oxidative Stress of Cardiomyocytes by Targeting MicroRNA-138-5p/MCU Axis: Implications for Diabetic Cardiomyopathy.
Liu X, Zhang Q, Zhang Y … +4 more , Dong J, Wang R, Zhang Q, Chen Y
Biochem Genet · 2025 Oct · PMID 41037192 · Publisher ↗
This study investigates the regulatory effects of long non-coding RNA H19 on miR-138-5p and their collective impact on mitochondrial oxidative stress injury in high glucose-exposed cardiomyocytes, while elucidating the u...
This study investigates the regulatory effects of long non-coding RNA H19 on miR-138-5p and their collective impact on mitochondrial oxidative stress injury in high glucose-exposed cardiomyocytes, while elucidating the underlying molecular mechanisms. The findings aim to establish a theoretical foundation for understanding the pathogenesis of diabetic cardiomyopathy. The expression levels of lncRNA H19, miR-138-5p, and MCU were quantified using RT-qPCR. H9c2 cardiomyocytes were exposed to high glucose (HG, 33 mM) in vitro to establish a diabetic cardiomyopathy (DCM) model. Regulatory targeting relationships between lncRNA H19 and miR-138-5p, as well as between miR-138-5p and mitochondrial calcium uniporter(MCU), were confirmed through dual-luciferase reporter assays. Levels of reactive oxygen species (ROS), superoxide dismutase (SOD) activity, and malondialdehyde (MDA) content were quantified to evaluate intracellular oxidative stress in cardiomyocytes. MCU protein expression was analyzed by western blotting. In DCM, H19 and MCU were downregulated; miR-138-5p was upregulated. H19 overexpression increased SOD activity and reduced ROS and MDA levels in HG-treated H9c2 cardiomyocytes. Dual-luciferase assays validated miR-138-5p binding to H19 and MCU 3'UTRs. miR-138-5p overexpression suppressed MCU protein expression. Rescue experiments demonstrated miR-138-5p overexpression or MCU silencing reversed H19-mediated oxidative stress attenuation in HG-stimulated cells. Overexpression of H19 attenuates oxidative stress by modulating the miR-138-5p/MCU axis in DCM, highlighting its potential as a diagnostic biomarker and/or therapeutic target for this condition.
Tanshinone I Represses Ferroptosis to Protect Against Steroid-Induced Osteonecrosis of the Femoral Head by Activating the Nrf2/SLC7A11 Axis.
Lu L, Zhou M, Zhang X … +1 more , Qin X
Biochem Genet · 2026 Jun · PMID 41026344 · Publisher ↗
We sought to explore how Tanshinone I (TsI) mediates ferroptosis in femur tissue in a rat model of steroid-induced osteonecrosis of the femoral head (SIONFH). Rats were given lipopolysaccharide and methylprednisolone to...
We sought to explore how Tanshinone I (TsI) mediates ferroptosis in femur tissue in a rat model of steroid-induced osteonecrosis of the femoral head (SIONFH). Rats were given lipopolysaccharide and methylprednisolone to develop a rat model of SIONFH and treated with 5 mg/kg or 10 mg/kg TsI or in combination with ferroptosis inhibitor Fer-1. After different treatments, bone parameters (BMD, BV/TV, Tb.N, Tb.Th, and Tb.Sp), the levels of osteoblast markers (RUNX2, BGLAP, and Osteopontin proteins), and ferroptosis markers (SLC7A11, GPX4, and ACSL4) in femur tissues were detected; Additionally, ferroptosis indicators Fe, MDA, and GSH in femur tissues were detected by corresponding commercial kits. Additionally, this research conducted experiments including TUNEL staining for the cell death rate in femur tissue and immunofluorescence for reactive oxygen species (ROS) detection. The levels of GPX4 (ferroptosis resistance marker), Nrf2, and SLC7A11 through PCR, Western blot, and immunohistochemistry experiments. Furthermore, lentivirus was delivered into SIONFH rats to knock Nrf2 or SLC7A11 down to investigates whether TsI mediated Nrf2/SLC7A11. BMD, BV/TV, Tb.N, and Tb.Th decreased while Tb.SP increased in SIONFH rats, with increased pathological damage to femoral tissue, reductions in expression of osteoblast markers, and increased positive TUNEL signal and cell death rate. Meanwhile, enhanced ferroptosis evidenced by relevant markers was noted in femur tissues. Low- and high-dose TsI treatment attenuated ferroptosis in femoral tissue, improved bone parameters and pathological lesions in SIONFH rats, with the high-dose group demonstrating more pronounced therapeutic effects. Similarly, Fer-1 treatment exerted a comparable protective effect to that of TsI. Mechanistically, low-dose or high-dose TsI treatment up-regulated Nrf2 and SLC7A11 levels, while down-regulation of Nrf2 or SLC7A11 partly compromised the aforementioned impacts of TsI. TsI may alleviate the pathological lesions of SIONFH rats by activating the Nrf2 signaling pathway, thereby promoting SLC7A11 expression and inhibiting ferroptosis in femoral tissue. TsI holds significant potential for therapeutic applications in the treatment of SIONFH.
Evaluation of Salivary, Plasma, and Tissue ITGB8 and MIAT-lncRNA Expression as a Biomarker in Oral Squamous Cell Carcinoma: A Cross-Sectional Study.
Khayamzadeh M, Ghaderian SMH, Garajei A … +3 more , Jolani MS, Tavassoli A, Khodaee P
Biochem Genet · 2026 Jun · PMID 41015604 · Publisher ↗
Squamous cell carcinoma of the lips and oral cavity (OSCC) contributes to 90% of the nonmelanocytic tumors of these anatomical regions. Liquid biopsy is a new, relatively noninvasive, and effective method for screening,...
Squamous cell carcinoma of the lips and oral cavity (OSCC) contributes to 90% of the nonmelanocytic tumors of these anatomical regions. Liquid biopsy is a new, relatively noninvasive, and effective method for screening, diagnosing, and classifying tumors. Considering the role of integrin β8 subunit (ITGB8) and Myocardial infarction-associated transcript (MIAT) lncRNA in the pathogenesis and progression of different types of cancer, we aimed to evaluate the probable differences in the level of expression of these two biomarkers in control and OSCC cases and evaluate their diagnostic potential as a biomarker in tissue and liquid samples (blood and saliva) biopsy. Tissue, blood, and saliva samples from 60 participants (30 in each study group) were obtained for precise evaluation. Using extracted RNA from the samples and PCR assay, the expression level of these biomarkers was measured in control and case group samples. Parametric and nonparametric tests were equipped for the evaluation of the results. ROC analysis was done to determine the diagnostic potential of these biomarkers. Our results claimed significant differences in the level of expression of ITGB8 and MIAT-lncRNA among our study cohorts' samples. The ROC analysis revealed the valuable potential of these factors in the diagnosis of disease in tissue and blood samples. The results of the analysis for the saliva samples suggest a satisfactory diagnostic value for ITGB8 but nonsignificant diagnostic value for the MIAT-lncRNA. ITGB8 and MIAT-lncRNA expression levels could be considered in the evaluation of suspicious oral cavity lesions, especially in the tissue and blood samples.
Detection of Vancomycin Resistance Enterococcus Species Holding Genes vanA, vanB, vanC1, vanC2, and vanC3 Isolated from Urinary Tract Infections.
Abbas KF, Motaweq ZY
Biochem Genet · 2026 Jun · PMID 41014403 · Publisher ↗
Enterococci were hospitalized and resistant to numerous antibiotics. The present research aimed to determine the Vancomycin sensitivity by disc and Minimum Inhibitory Concentrations (MICs), also detecting the relationshi...
Enterococci were hospitalized and resistant to numerous antibiotics. The present research aimed to determine the Vancomycin sensitivity by disc and Minimum Inhibitory Concentrations (MICs), also detecting the relationship between Vancomycin resistance genes and the Vancomycin resistance in uropathogenic Enterococcus species. Totally, 150 urine specimens were obtained from patients who attended or admitted to Iraq hospitals. The bacteriological tests besides Vietic and (ddl of E. faecalis, ddl of E. faecium) genes were implemented for the identification of Enterococcus isolates. We indicate 27 Enterococcus isolates, among which 18 (66.7%) were E. faecalis, 4 (14.8%) were E. faecium, while 5 (18.5%) were other isolates belonging to the rest of Enterococcus species. The antibiotic resistance by disk-diffusion technique for Penicillin, Ampicillin, Vancomycin, Norfloxacin, Erythromycin, Ciprofloxacin, Rifampin, Levofloxacin, Chloramphenicol, Fosfomycin, Doxycycline, Minocycline, and Nitrofurantoin was 7 (25,92%), 7 (25,92%), 6 (22.22%), 5 (18.51%), 24 (88.89%), 5 (18.51%), 23 (85.18%), 5 (18.51%), 4 (14.81%), 14 (51.85%), 0 (0%), 3 (11.11%), and 1 (3.70%), respectively. The total isolates were Vancomycin Resistance Enterococci VRE using the MIC technique. Positive results for vanA 23 (85.18%), vanB 11 (40.74%), vanC1 3 (11.11%), vanC2, and vanC3 3 (11.11%). The results revealed that 23 (85.18%) out of VRE isolates possessed the Vancomycin-resistance genes. Although four isolates did not hold van genes, the resistance may be attributed to the occurrence of uncommon genes which not identified by this study; also the efflux pump has a role in resistance. The van genes might be transmitted, so important to monitor antibiotic resistance.
FTO-Mediated m6A Demethylation of MZF1 Regulates DECR1 to Promote Fatty Acid Oxidation and Exacerbate Myocardial Ischemia/Reperfusion Injury : FTO-Mediated m6A Demethylation of MZF1 Enhances Fatty Acid Oxidation and Aggravates Myocardial I/R Injury.
Tian J, He Q, Li N … +3 more , Sun Y, Zhang A, Wang H
Biochem Genet · 2026 Jun · PMID 41003915 · Publisher ↗
Myocardial ischemia-reperfusion injury (MIRI) is a major clinical challenge, marked by metabolic disruptions and cellular damage following the restoration of blood flow after ischemia. During ischemia, the heart shifts f...
Myocardial ischemia-reperfusion injury (MIRI) is a major clinical challenge, marked by metabolic disruptions and cellular damage following the restoration of blood flow after ischemia. During ischemia, the heart shifts from fatty acid metabolism to glucose metabolism, leading to metabolic abnormalities, including reduced intracellular pH, ion disturbances, cell swelling, and apoptosis. Upon reperfusion, fatty acid β-oxidation resumes, becoming the dominant energy source, which induces excessive oxidative stress and aggravates myocardial injury. To explore the role of FTO (Fat mass and obesity-associated protein) in m6A demethylation of MZF1 and its regulation of DECR1, a key enzyme involved in fatty acid β-oxidation, in the context of MIRI. We investigated the molecular mechanisms by which FTO-mediated m6A modification of MZF1 regulates DECR1 expression, leading to enhanced fatty acid oxidation during reperfusion and its contribution to the exacerbation of MIRI. Our findings suggest that FTO-mediated demethylation of MZF1 promotes the expression of DECR1, thereby enhancing fatty acid oxidation. This process intensifies oxidative stress and worsens myocardial injury during ischemia/reperfusion. The FTO-mediated m6A modification of MZF1 represents a critical mechanism in the regulation of fatty acid oxidation and the exacerbation of MIRI. These insights offer potential therapeutic targets to mitigate the harmful effects of reperfusion injury in myocardial infarction.
Mechanistic Insights into Systemic Targets of Magnolia Mediating Beneficial Effects in Metabolic Syndrome through Biochemical and In Situ Analyses.
Oflaz O, Turan B
Biochem Genet · 2026 Jun · PMID 40986232 · Publisher ↗
Metabolic syndrome (MetS) is characterized by a cluster of biochemical and physiological abnormalities. Healthy eating, including the consumption of natural products, holds promise for promoting health and preventing dis...
Metabolic syndrome (MetS) is characterized by a cluster of biochemical and physiological abnormalities. Healthy eating, including the consumption of natural products, holds promise for promoting health and preventing disease. Among these, Magnolia officinalis bark extract (MAGBE) is widely used as a dietary supplement due to its potent antioxidant, anti-inflammatory, and neuroprotective properties. In this study, we aimed to investigate the therapeutic potential of MAGBE in a rat model of MetS and to identify its target proteins. One group of 2-month-old male Wistar rats was supplemented with MAGBE (400 mg/kg/day, administered intragastrically) for 16 weeks alongside a high-carbohydrate diet (containing 32% sucrose) (MetS + MAGBE group). A second group received only the high-carbohydrate diet for the same period (MetS group), while a third group was maintained under standard conditions (Control group). Following confirmation of MetS induction in experimental animals, MAGBE treatment significantly improved elevated systolic and diastolic blood pressure, as well as heart rate. It also provided significant benefits in terms of oxidative stress/antioxidant balance and anti-inflammatory status, along with improved plasma levels of leptin, IL-6, IL-10, TNF-α, and leukotriene B4 (LTB₄), a product of arachidonate 5-lipoxygenase (ALOX5). Furthermore, in silico molecular docking approaches identified several potential protein targets of MAGBE, including the cannabinoid receptors CB₁ and CB₂. These receptors play central roles in regulating appetite and energy balance by modulating metabolic processes, as well as in immune function by suppressing cytokine production. Additionally, our analysis revealed strong interactions between MAGBE and the active site of ALOX5, which catalyzes the conversion of arachidonic acid into proinflammatory molecules such as LTB₄, a key mediator of inflammation and immune response. Overall, our findings highlight the beneficial antioxidant and anti-inflammatory effects of MAGBE in the prevention of MetS-associated disorders, potentially through interactions with receptors such as cannabinoid CB₁/CB₂ and ALOX5.Impact StatementIncreasing evidence supports the rapid rise in the prevalence of metabolic syndrome (MetS) across populations, contributing to the development of various organ dysfunctions and type 2 diabetes. Given the importance of healthy nutrition with natural compounds, we demonstrated the beneficial effects of Magnolia officinalis bark extract (MAGBE) even under a high-carbohydrate diet by analyzing systemic physiological parameters. MAGBE treatment restored heart function as well as plasma biomarkers related to oxidative stress/antioxidant balance and anti-inflammatory status, despite elevated blood glucose and plasma insulin levels. Using in silico molecular docking approaches, we identified several protein targets through which MAGBE may exert its effects, including cannabinoid receptors CB₁ and CB₂, central regulators of appetite, energy balance, and immune response via cytokine suppression, and the active site of ALOX5, which catalyzes the production of leukotriene B₄ (LTB₄), a key proinflammatory mediator in immune responses.
Propofol Inhibits Lung Cancer Glycolysis by Influencing the Deubiquitination Modification of TPI1 Regulated by USP5.
Wang Y, Zhou H, Guo W … +2 more , Xu J, Miao C
Biochem Genet · 2026 Jun · PMID 40956511 · Publisher ↗
BACKGROUND: Lung cancer is a malignant tumor of the bronchial mucosa or gland, the morbidity and mortality increase rapidly, and it is a great threat to human health and life. Propofol is a short-acting intravenous anest...
BACKGROUND: Lung cancer is a malignant tumor of the bronchial mucosa or gland, the morbidity and mortality increase rapidly, and it is a great threat to human health and life. Propofol is a short-acting intravenous anesthetic, and its effect on lung cancer has been studied, but the mechanism is not thorough. METHODS: The 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazoliumromide (MTT), 5-ethynyl-2'-deoxyuridine (EdU) staining, flow cytometry, and transwell assays were applied to assess the viability, proliferation, apoptosis, and invasion, respectively. The glycolytic analysis was performed using the corresponding kits. The gene expression was evaluated by quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot. The interaction between genes was obtained from the STRING database or ubiquitination analysis. The xenograft tumor mouse models were established to verify the effects of propofol in vivo, and IHC was adopted to detect the gene expression in vivo. RESULTS: In this study, we found that propofol impeded lung cancer progression and glycolysis. Additionally, propofol curbed the triosephosphate isomerase 1 (TPI1) protein and increased TPI1 ubiquitination modification, meanwhile, propofol exerted inhibitory functions in lung cancer through TPI1. Besides, the protein stability and ubiquitination modification of TPI1 were mediated by ubiquitin-specific peptidase 5 (USP5), and USP5 expedited the progression and glycolysis of lung cancer via TPI1. In the meantime, propofol modulated USP5-regulated functions in lung cancer. In vivo, propofol-inhibited tumor growth by regulating USP5-mediated TPI1. CONCLUSION: This study presents propofol/USP5/TPI1 curbing glycolysis metabolism and tumor growth in lung cancer, indicating that propofol-mediated ubiquitination of the target gene may be a new therapeutic target for lung cancer.
Knockdown of Long Non-coding RNA-MALAT1 Ameliorates Diabetic Lower Limb Atherosclerotic Disease Through MiR-17-5p-Mediated Endothelial Cell Pyroptosis.
Li J, Xu JX, Wang C … +1 more , Zhu FF
Biochem Genet · 2026 Jun · PMID 40947474 · Publisher ↗
We observed the expression of long non-coding RNA (lncRNA) MALAT1 and microRNA (miR)-17-5p in patients with diabetic lower extremity atherosclerosis (LEAD) and EA. hy926 human endothelial cells (EA. Hy926 cells). We furt...
We observed the expression of long non-coding RNA (lncRNA) MALAT1 and microRNA (miR)-17-5p in patients with diabetic lower extremity atherosclerosis (LEAD) and EA. hy926 human endothelial cells (EA. Hy926 cells). We further investigated whether knockdown of MALAT1 (sh-MALAT1) could protect endothelial cells and improve the occurrence of atherosclerosis through miR-17-5p, aiming to dissect the underlying mechanism. Patients with type 2 diabetes were stratified into two groups: those with lower extremity atherosclerotic lesions (LEAD group) and those without (T2DM group). For in vitro studies, EA. hy926 cell cultures were treated with high glucose concentrations and transfected. The mRNA expression levels of MALAT1 and miR-17-5p were accessed. The relationship between molecules was verified by double luciferase assay. Biological function was evaluated using lactate dehydrogenase (LDH) assay, Hoechst 33342/propidium iodide (PI) fluorescence staining, and Western blotting. MALAT1 was highly expressed and miR-17-5p was lowly expressed in both peripheral blood samples from LEAD patients and high glucose-cultured endothelial cells. Knockdown of MALAT1 (sh-MALAT1) or miR-17-5p mimic attenuated the release of LDH, the levels of pyroptosis-associated protein, and the number of PI-positive cells in high glucose-treated endothelial cells, while the miR-17-5p inhibitors had the opposite effect. The dual-luciferase assay determined that miR-17-5p is a downstream target of MALAT1. Finally, co-transfection with sh-MALAT1 and miR-17-5p inhibitors attenuated the protective effect of silenced MALAT1 on high glucose-mediated endothelial cell pyroptosis. MALAT1 may play an essential role in high glucose-induced endothelial cell pyroptosis by regulating miR-17-5p.
Dihuang Yinzi Ameliorates Cognitive Impairments and Inhibits Ferroptosis in APP/PS1 Mice.
Xie F, Zhou L, Yu M
Biochem Genet · 2026 Jun · PMID 40938517 · Publisher ↗
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and neuronal loss. Ferroptosis, a form of regulated cell death driven by iron overload and lipid peroxidation, has b...
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and neuronal loss. Ferroptosis, a form of regulated cell death driven by iron overload and lipid peroxidation, has been implicated in AD pathology. DiHuangYinZi (DHYZ), a traditional Chinese herbal remedy, has been suggested to ameliorate cognitive impairments and reduce ferroptosis in AD models. This study aimed to investigate the effects of DHYZ on learning, memory, ferroptosis markers, and neuronal integrity in APP/PS1 transgenic mice. Six-month-old APP/PS1 transgenic mice were treated with DHYZ or donepezil for four weeks. Learning and memory functions were evaluated using the Morris Water Maze (MWM) and open field test. Neuronal integrity was assessed through Hematoxylin and Eosin (H&E) and Nissl staining. Ferroptosis markers, including superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and the GSH/GSSG ratio, were measured in hippocampal tissues. Ferroptosis-related protein expressions, such as ferritin, DMT1, FPN1, Nrf2, and GPX4, were analyzed using Western blot. DHYZ treatment significantly improved learning and memory deficits in APP/PS1 mice, as evidenced by reduced escape latency and increased platform crossings in the MWM. DHYZ also reversed anxiety-like behavior in the open field test. Histological analysis showed that DHYZ treatment restored neuronal integrity, as indicated by better cellular arrangement and staining compared to untreated APP/PS1 mice. DHYZ inhibited ferroptosis by reducing iron overload, increasing SOD and GSH levels, and normalizing the GSH/GSSG ratio. Moreover, DHYZ modulated the expression of ferroptosis-related proteins, restoring FPN1 levels while reducing ferritin and DMT1 expressions. Nrf2 and GPX4 levels, which were reduced in APP/PS1 mice, were significantly increased after DHYZ treatment. DHYZ effectively improved cognitive deficits, inhibited ferroptosis, and restored neuronal integrity in APP/PS1 mice. These findings suggest that DHYZ may have therapeutic potential for AD by targeting ferroptosis and regulating iron metabolism.
The Complete Chloroplast Genome of Tree Fern Cyathea delgadii and Its Comparison to Other Cyatheales.
Metz GF, Ferreira TV, Ferreira RV … +3 more , Matielo CBD, Lemos RPM, Victoria FC
Biochem Genet · 2026 Jun · PMID 40936070 · Publisher ↗
The chloroplast (cp) genome of the tree fern Cyathea delgadii Pohl ex Sternb. was assembled and annotated to investigate its structure and evolution within the Cyatheales order. The genome, sequenced using Oxford Nanopor...
The chloroplast (cp) genome of the tree fern Cyathea delgadii Pohl ex Sternb. was assembled and annotated to investigate its structure and evolution within the Cyatheales order. The genome, sequenced using Oxford Nanopore Technologies, has a total size of 165,248 bp, comprising a large single-copy (LSC) region of 94,738 bp, a small single-copy (SSC) region of 22,012 bp, and two inverted repeat (IR) regions of 24,251 bp each. It contains 89 protein-coding genes, eight rRNAs, and 33 tRNAs. Comparative phylogenomic analyses involving 19 species of Cyatheales have revealed that the cp genome of C. delgadii shares similarities in gene content with other ferns of the Cyatheaceae family; however, it demonstrates variations in both genome size and GC content. Variations in cp genome size were observed across the Cyatheales species, ranging from 154,046 bp in Gymnosphaera denticulata (Baker) Copel to 168,244 bp in Dicksonia squarrosa (G.Forst) SW. Gene content analysis showed that most species have a conserved number of protein-coding genes, rRNAs, and tRNAs, suggesting structural stability. However, Cibotium spp. has a reduced number of protein-coding genes (87), possibly due to gene loss or transfer to the nuclear genome. Phylogenetic analyses using both whole genome and SNP data showed comparable clustering among Alsophila and Gymnosphaera species, while C. delgadii occupied a basal to intermediate position. The overall guanine-cytosine (GC) content of C. delgadii was calculated to be 40.95%, with a significantly higher content of 44.03% observed in the intragenic regions. An analysis of codon usage bias indicated a preference for codons ending with adenine or thymine, which aligns with the genome's adenine-thymine (AT) richness. This study provides valuable genomic resources and insights into the evolution of Cyatheales cp genomes, emphasizing both conserved features and specific adaptations within this group of ferns.
Exploring Differentially Expressed Genes and Understanding the Underlying Mechanisms in Glioblastoma.
Seven D, Ekici A, Uebe S … +5 more , Bilgiç B, Sencer A, Aydoseli A, Reis A, Buyru N
Biochem Genet · 2026 Jun · PMID 40931220 · Publisher ↗
Glioblastoma is the most aggressive and malignant tumor of the central nervous system. Current treatment options, including surgical excision, radiotherapy, and chemotherapy, have Limited efficacy, with a median survival...
Glioblastoma is the most aggressive and malignant tumor of the central nervous system. Current treatment options, including surgical excision, radiotherapy, and chemotherapy, have Limited efficacy, with a median survival rate of approximately 15 months. To develop novel therapeutics, it is crucial to understand the underlying molecular mechanisms driving glioblastoma. However, obtaining healthy tissue counterparts for comparison is often challenging due to the critical nature of the tissues and the tumor's location. This study aimed to compare the transcriptomic profiles of glioblastoma tissues with those of adjacent healthy tissues, to elucidate key pathways and identify upstream regulators involved in glioblastoma pathogenesis. Twenty-six pairs of glioblastoma tissues and their adjacent healthy tissues were obtained during surgery. The tumor and healthy origins were confirmed through histopathological examination. Twelve pairs were analyzed via transcriptome analysis by using the Ion GeneStudio S5 system. Ingenuity pathway analysis was performed to identify the associated pathways and upstream regulators. Selected 51 upstream regulators were analyzed using qRT-PCR. Three pairs were excluded from the RNA-sequencing (RNA-seq) analysis due to similarities between normal and tumor tissues. The dysregulated pathways were primarily associated with neuronal connections and neurotransmitter pathways. The expression patterns of upstream regulators were consistent with RNA-seq results. Molecular changes linked to the initiation of tumors can begin at an early stage, potentially preceding the appearance of clinical symptoms. The dysregulated pathways were particularly associated with specific brain tissue types. The expression of upstream regulators was consistent across both methods; however, their functional roles need further investigation.
Upregulation of Hsa_circ_0077007 Expression is Used for Prognosis and Targeted Therapy of Colorectal Cancer.
Zhang X, Lu J
Biochem Genet · 2026 Jun · PMID 40924303 · Publisher ↗
To evaluate the expression of hsa_circ_0077007 in the serum of colorectal cancer (CRC) patients and offer a foundational theory for the prognosis of CRC. The present study focuses on investigating the biological function...
To evaluate the expression of hsa_circ_0077007 in the serum of colorectal cancer (CRC) patients and offer a foundational theory for the prognosis of CRC. The present study focuses on investigating the biological function and therapeutic target of hsa_circ_0077007 in colorectal cancer CRC. Retrieve the GEO database and use the GEO2R tool to analyze the GSE dataset (GSE223001 and GSE159669) to obtain aberrantly expressed circRNAs. Serum hsa_circ_0077007 expression was measured by qRT-PCR in 107 CRC patients. Kaplan-Meier curve was used to analyze the repercussions of hsa_circ_0077007 expression on overall survival and prognosis. After the knockout of hsa_circ_0077007, the biological cellular functions of CRC were characterized. Finally, the downstream molecular expression mechanism of hsa_circ_0077007 was further explored. Hsa_circ_0077007 was among the abnormal circRNAs in GSE223001 and GSE159669. Compared to normal controls, CRC patients exhibited elevated levels of hsa_circ_0077007 expression in their serum. Additionally, the expression levels of hsa_circ_0077007 were significantly increased across four distinct CRC cellular lines, especially SW620 and LoVo cellular lines. Furthermore, high levels of hsa_circ_0077007 expression were associated with a reduced overall survival rate. In vitro, loss-of-function assays for hsa_circ_0077007 resulted in a marked reduction in cell proliferation, invasion, and migration, accompanied by a boost in cell apoptosis. Hsa_circ_0077007 can sponge miR-383-5p, and then inhibit the expression of miR-383-5p. High expression of hsa_circ_0077007 is indicative of shorter survival rates among CRC patients. The hsa_circ_0077007 has been demonstrated to enhance cellular proliferation, invasion, and migration, while concurrently inhibiting apoptosis.
Exploring EZH2-Linked lncRNAs in Gastric Cancer: Insights from Sequencing Data and Gene Modulation.
Masoudi Kazemabad A, Safaralizadeh R, Haghi M … +1 more , Forghanifard MM
Biochem Genet · 2026 Jun · PMID 40913693 · Publisher ↗
Gastric cancer (GC) is one of the leading causes of cancer-related deaths globally. Enhancer of zeste homolog 2 (EZH2), a methyl-transferase and master transcriptional regulator frequently overexpresses in a variety of m...
Gastric cancer (GC) is one of the leading causes of cancer-related deaths globally. Enhancer of zeste homolog 2 (EZH2), a methyl-transferase and master transcriptional regulator frequently overexpresses in a variety of malignancies. Long non-coding RNAs (lncRNAs) play a significant role in regulating gene expression and are intricately involved in the EZH2 oncogenic regulatory network. We aimed in this study to investigate the expression of EZH2-associated lncRNAs and their probable regulatory role in GC progression. RNA-seq and miRNA-seq data from 375 tumor and 32 normal samples were retrieved from the TCGA database. Differential expression and correlation analyses were performed to identify EZH2-associated lncRNAs. A competing endogenous RNA (ceRNA) network comprising lncRNAs, miRNAs, and mRNAs was constructed and visualized. Functional genomics analysis including EZH2 knockdown and induced overexpression experiments were carried out in AGS and MKN-45 GC cell lines to validate the expression of selected lncRNAs using RT-qPCR. EZH2-correlated analysis revealed 16 upregulated and 8 downregulated lncRNAs with significant associations. EZH2 expression modulation studies confirmed that expression levels of lncRNAs including PVT1, MNX1-AS1, AC103702.2, PCAT7, LINC01235, LINC02086, MIR99AHG, and MAGI2-AS3 were regulated by EZH2 in GC cells. EZH2 modulates the expression of several key lncRNAs associated with gastric cancer progression, suggesting that the EZH2/lncRNA axis could serve as a potential therapeutic target. Targeting this axis may open new avenues for influencing critical molecular pathways involved in GC development.
Cuproptosis-Related Gene FDX1 Induces Malignant Progression and Immune Suppression in Triple-Negative Breast Cancer.
Sun H, Chen Q, Zhang X … +3 more , Chen M, Dai J, Yan M
Biochem Genet · 2026 Jun · PMID 40911146 · Publisher ↗
Triple-negative breast cancer (TNBC), a particularly aggressive cancer, significantly menaces women's health. Recently, a novel form of cell death known as cuproptosis has been identified, with the key gene FDX1 emerging...
Triple-negative breast cancer (TNBC), a particularly aggressive cancer, significantly menaces women's health. Recently, a novel form of cell death known as cuproptosis has been identified, with the key gene FDX1 emerging as a potential oncogenic factor. We analyzed the heterogeneity of breast cancer (BC) epithelial cells using available single-cell RNA sequencing (scRNA-seq) datasets. We developed knockdown cell lines in vitro and verified the knockdown efficiency with qPCR. The malignant phenotypes of the cells were assessed through cell counting kit-8, colony formation, Transwell, and scratch healing assays. We also co-cultured the cells with CD8 T cells and evaluated their activation using Transwell, CFSE, lactate dehydrogenase release assay, and enzyme-linked immunosorbent assay. IHC analysis was conducted to reveal the impact of FDX1 on tumor growth in mice. Based on scRNA-seq data, we discovered that in TNBC, epithelial cells were more abundant, and T-cell infiltration was less frequent compared to other subtypes of BC. FDX1 + epithelial cells, which are associated with cuproptosis, were highly enriched in TNBC. The expression of FDX1, a key gene in cuproptosis, upregulated in these cells. This upregulation is essential for sustaining the growth, invasion, and migration of TNBC cells. Co-culture experiments revealed that FDX1 expression could modulate the activation and cytotoxicity of T cells. Tumor growth in mice was largely curbed by the knockdown of FDX1 expression. In TNBC, FDX1 expression aids in the survival and proliferation of cancer cells while dampening the immune response of CD8 T cells.
Correction: LncRNA XIST Protects Against Polycystic Ovary Syndrome via the Regulation of miR-212-3p/RASA1 Axis.
Xu X, Yin C, Dong B … +3 more , Li Y, Liu S, Chen J
Biochem Genet · 2025 Oct · PMID 40906218 · Publisher ↗
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