Biochemical Genetics[JOURNAL]
Sun
200 papers
CAECC-Subtyper: A Novel Convolutional Autoencoder Framework for Integrating Multi-omics Data in Cancer Subtyping.
Uyar H, Gumus O
Biochem Genet · 2025 Dec · PMID 41343001 · Publisher ↗
Cancer is a complex group of diseases characterized by diverse molecular alterations, including genomic, epigenetic, and transcriptomic changes, which vary across different cancer types. This heterogeneity complicates th...
Cancer is a complex group of diseases characterized by diverse molecular alterations, including genomic, epigenetic, and transcriptomic changes, which vary across different cancer types. This heterogeneity complicates the development of standardized treatments, making the accurate identification of cancer subtypes crucial for enabling targeted therapies and improving patient outcomes. In this study, we present CAECC-Subtyper, a novel framework for cancer subtyping that integrates multi-omics data for the clustering of cancer patients. The proposed approach incorporates convolutional autoencoder and consensus clustering modules. The convolutional autoencoder was employed to extract relevant features from the multi-omics datasets, which were then used in consensus clustering to cluster patients into distinct subtypes. We utilized multi-omics data, including mRNA, miRNA, lncRNA, methylation, and protein profiles of breast cancer patients obtained from The Cancer Genome Atlas. The clusters identified through the CAECC-Subtyper framework were evaluated for survival differences using the log-rank test, revealing statistically significant variations. The performance of the proposed method was compared to existing techniques in the literature, demonstrating its superior or competitive performance. Furthermore, the generalizability and prognostic significance of the method were evaluated on three external datasets, confirming a highly significant prognostic value in the external breast cancer cohort. Biomarkers specific to the identified breast cancer subtypes were discovered through differential gene expression analysis and the Minimum Redundancy Maximum Relevance algorithm, with their clinical relevance further supported by existing literature.
KIAA1429 Stabilizes FAM84B mRNA to Enhance Colorectal Cancer Tumorigenesis via Wnt/β-Catenin Pathway.
Lu Y, Wang W, Peng L … +1 more , Wang Z
Biochem Genet · 2025 Dec · PMID 41329451 · Publisher ↗
Colorectal cancer (CRC) is a relatively widespread malignancy that contributes to considerable mortality and healthcare challenges. Recent studies emphasize the significance of N6-methyladenosine (mA) RNA modification in...
Colorectal cancer (CRC) is a relatively widespread malignancy that contributes to considerable mortality and healthcare challenges. Recent studies emphasize the significance of N6-methyladenosine (mA) RNA modification in CRC progression. However, research on KIAA1429 (a key mA methyltransferase) is still limited during CRC. This study focuses on investigating the impact of KIAA1429-driven mA modification on CRC progression. The expression of KIAA1429 in CRC was assessed via bioinformatics analyses and qRT-PCR methods. Its impact on CRC cell malignancy was examined by employing CCK8, colony formation, wound healing, and transwell invasion assays. The relationship among KIAA1429 and Family with sequence similarity 84, member B (FAM84B) was verified via qRT-PCR, immunoblotting, and MeRIP. Finally, the effect of their interaction on CRC cell malignancy and Wnt/β-catenin signaling was assessed in vitro and in vivo. The KIAA1429 expression was markedly high in CRC, and silencing it significantly reduced malignant phenotypes of CRC cells. The bioinformatics analysis identified FAM84B as a target gene of KIAA1429 in CRC, with elevated expression and mA-dependent methylation regulation by KIAA1429. The outcomes of qRT-PCR, immunoblotting and MeRIP assay confirmed a positive association between KIAA1429 and FAM84B. Furthermore, KIAA1429 silencing partially decreased β-catenin levels and reversed the malignant effects of FAM84B overexpression on CRC cells, both in vitro and in vivo. The results illustrate that KIAA1429 promotes CRC tumorigenesis by stabilizing FAM84B mRNA and activating the Wnt/β-catenin pathway, highlighting its capability as a prognostic biomarker and therapeutic target for CRC.
MicroRNA-Mediated Post-transcriptional Regulation of Wood Property Traits in Eucalyptus tereticornis.
Madhuvanthi CK, Bhuvanam S, Muthupandi M … +1 more , Ghosh Dasgupta M
Biochem Genet · 2025 Dec · PMID 41324866 · Publisher ↗
Eucalyptus is a fast growing hardwood tree species preferred for its wood properties which are suitable for paper and pulp industries. The transcriptional regulation governing secondary wood formation in Eucalyptus is ex...
Eucalyptus is a fast growing hardwood tree species preferred for its wood properties which are suitable for paper and pulp industries. The transcriptional regulation governing secondary wood formation in Eucalyptus is extensively studied while the role of post-transcriptional mechanism determining wood phenotypes is not well documented. The present study aimed at understanding the miRNA-mediated regulation of secondary development in Eucalyptus tereticornis. Transcriptome-wide identification of miRNAs in wood tissues predicted a total of 266 conserved mature miRNA members belonging to 76 families. Et-miR156 was the most abundant family followed by Et-miR166 and Et-miR167. Majority of the gene targets of miRNAs were transcription factors including AP2, GRF, TCP, ARF, bHLH, bZIP, HD-ZIP, MYB, NAC, SBP, WRKY and Zinc finger. Further, 102 miRNA members were predicted to target genes from the cellulose and lignin biosynthetic pathways. Additionally, the expression patterns of four miRNAs (Et-miR156d-5p, Et-miR156a, Et-miR156b-5p, and Et-miR159b) and their gene targets were validated in eight individuals with contrasting cellulose and lignin content to predict the role of miRNAs in governing wood property traits. In summary, the present study has predicted potential miRNA targets which may regulate wood phenotypes in E. tereticornis and has also generated valuable genomic resource for enhancing wood quality through marker assisted selection and gene editing strategies.
Evaluation of Phytochemical Variations Among the Different Genotypes of Black Turmeric (Curcuma caesia Roxb.).
Isha V, Venkatesan K, Rajashree V … +3 more , Senthil N, Renuka R, Chandrakumar K
Biochem Genet · 2025 Nov · PMID 41317210 · Publisher ↗
Black turmeric (Curcuma caesia Roxb.) is widely used in traditional medicine due to its antifungal, antibacterial, anticancer, analgesic, anti-inflammatory, and anticonvulsant properties. Despite these properties, system...
Black turmeric (Curcuma caesia Roxb.) is widely used in traditional medicine due to its antifungal, antibacterial, anticancer, analgesic, anti-inflammatory, and anticonvulsant properties. Despite these properties, systematic phytochemical evaluation of different genotypes remains limited. This study investigated the biochemical diversity of 21 genotypes collected from different agro-climatic regions of India and cultivated under a randomized block design at two distinct environments- Bhavanisagar and Coimbatore, Tamil Nadu, India. Methanolic extracts of rhizomes were quantitatively assessed for total phenolics, flavonoids, proteins, alkaloids, and cardiac glycosides. The analysis revealed significant variation attributable to both genotypic differences and environmental conditions. At Bhavanisagar, genotype GCA-5 recorded the highest phenolic (3.81 mg GAE/g DW) and cardiac glycoside (183.38 mg SE/g) contents, whereas GMN-10 exhibited the maximum flavonoid concentration (38.29 mg QE/g). The highest protein content was observed in GAN-16 (165.86 mg/100 g DW), while GTE-18 showed the greatest alkaloid accumulation (227.34 mg AE/g). Notably, GTE-18 also ranked among the top performers across most traits at Coimbatore, indicating its strong stability across environments. Correlation analysis revealed a significant positive relationship between cardiac glycosides and phenols (r = 0.49**), proteins (r = 0.40**), and flavonoids (r = 0.34**), as well as between flavonoids and antioxidant capacity (r = 0.59**) and proteins (r = 0.22**), suggesting coordinated biosynthesis. These interrelationships highlight potential metabolic linkages and support the pharmacological synergy of secondary metabolites. Genotypes GCA-5, GTE-18, and GMN-10 demonstrated superior phytochemical accumulation and adaptability across environments, indicating their potential for pharmaceutical and nutraceutical applications.
The SP1/NEDD4L Axis Suppresses the Breast Cancer Progression by Downregulating SNAI2 Expression.
Zuo B, Li X, Wang M … +10 more , Yin Z, Guo Y, Zhao L, Yang R, Tong B, Guo Z, Sun M, Zhao J, Zhang H, Li G
Biochem Genet · 2025 Nov · PMID 41307818 · Publisher ↗
While NEDD4L is implicated in the onset and progression of various tumors, its role in breast cancer (BRCA) remains unclear. This study aimed to clarify the molecular mechanism behind NEDD4L expression in BRCA and its im...
While NEDD4L is implicated in the onset and progression of various tumors, its role in breast cancer (BRCA) remains unclear. This study aimed to clarify the molecular mechanism behind NEDD4L expression in BRCA and its impact on prognosis. TCGA_BRCA, METABRIC, GSE24450 and GSE42568 data sets were used for gene expression and survival analysis. The riskscore model was developed by LASSO Cox regression, and the nomogram was constructed based on the BRCA riskscore and clinical characters. Cell proliferation and migration were assessed using CCK-8, plate clone formation, and transwell assays. Detection of target genes was achieved using Western blots, immunohistochemistry, and immunofluorescence. Statistical and survival analyses showed that NEDD4L was significantly reduced in BRCA, correlating with poor prognosis. Knockdown of NEDD4L can significantly enhance BRCA cell proliferation and migration. Bioinformatics, cytological experiments, and human BRCA tissue chip analysis reveal that SP1 mediates the reduction of SNAI2 expression in BRCA by promoting NEDD4L expression. The NEDD4L-based LASSO Cox regression model represents an independent prognostic factor. A quantitative evaluation of BRCA prognosis was achieved using a nomogram that integrates risk scores with clinical indicators. This study provides evidence for the SP1/NEDD4L/SNAI2 signal axis mechanism in BRCA, and developed a reliable prognosis model, providing a new target for BRCA therapy. Targeting this axis may lead to innovative treatments, including combination therapies, and help identify new biomarkers for early detection and monitoring of BRCA.
Development of Knockout Cardiac Muscle Cell Lines Using Integrase-Deficient Lentivirus-Mediated CRISPR/Cas9 Gene Editing.
Zhang F, Lu Q, Qian X … +2 more , Xing Y, Wang W
Biochem Genet · 2025 Nov · PMID 41307817 · Publisher ↗
Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing technology is a highly efficient genome editing tool that can genetically disrupt genes and genetic eleme...
Clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) gene editing technology is a highly efficient genome editing tool that can genetically disrupt genes and genetic elements, making it a timely, cost-effective, and powerful tool for studying gene function. The success of gene editing depends on the ability to introduce CRISPR components, including guide RNA (gRNA) and Cas9 nuclease, into the target cell, which is challenging in numerous difficult-to-transfect cell types, such as cardiomyocytes. Lentiviral vectors (LVs) are among the primary delivery methods for the CRISPR/Cas9 system as they can stably maintain robust expression in various dividing and non-dividing cells. However, stably integrated LVs consistently express CRISPR/Cas9 components at high levels, rendering them susceptible to off-target effects. New-generation integrase-deficient LV (IDLV) offers an attractive alternative approach for delivering CRISPR/Cas9 components. This study constructed transient receptor potential cation channel mucolipin subfamily member 1 gene knockout models in H9C2 cell lines using IDLVs. Strategies for gRNA design and screening, the IDLV packaging process, CRISPR delivery, and knockout validation are outlined. These protocols will assist researchers in the application of CRISPR technology to study gene function in mammalian cells.
Whole-Exome Sequencing Identified a Nonsense Pathogenic Variant in the MITF Gene Associated with Non-syndromic Hearing Loss.
Soleimani F, Pooladi A, Alasvand M … +2 more , Karbasi G, Fathi F
Biochem Genet · 2025 Nov · PMID 41307816 · Publisher ↗
Hearing loss exhibits significant clinical and genetic heterogeneity. More than 50% of Hearing loss cases have a genetic etiology. In terms of genetics,, hearing loss can be classified as either syndromic or non-syndromi...
Hearing loss exhibits significant clinical and genetic heterogeneity. More than 50% of Hearing loss cases have a genetic etiology. In terms of genetics,, hearing loss can be classified as either syndromic or non-syndromic. It has been demonstrated that over 100 genes and 1,000 associated mutations are involved in hearing loss that can be inherited through autosomal recessive, autosomal dominant, X-linked, or mitochondrial mechanisms This vast genetic heterogeneity has posed a significant challenge for genetic researchers in identifying the specific mutated gene in affected individuals from diverse ethnic backgrounds. However, recent advancements in next-generation sequencing technologies, particularly whole-exome sequencing (WES), have facilitated the identification of mutated genes in individuals with deafness. The primary objective of this study was to employ whole-exome sequencing (WES) to ascertain the genetic underpinnings of non-syndromic hearing loss in a Kurdish consanguineous family and to examine the associated clinical manifestations of the identified genetic mutation. A cohort of fifteen affected (fourteen with prelingual and one with postlingual hearing loss) and fifteen unaffected individuals from a Kurdish family was enrolled in this study. A comprehensive evaluation was conducted, encompassing meticulous physical examinations and audiometric assessments, to ascertain the presence of hearing impairment among the affected participants. Genomic DNA was extracted from blood samples and subjected to whole-exome sequencing. Subsequent variant identification and annotation were conducted to identify potential pathogenic mutations. To corroborate the finding of whole-exome sequencing (WES), a polymerase chain reaction (PCR) was performed on the flanking region encompassing the identified variant. Subsequent Sanger sequencing of the PCR product verified the presence of the WES-derived variant. The variant was than investigated in additional affected families through Sanger sequencing and restriction fragment length polymorphism (RFLP)-PCR analysis. A thorough analysis of whole-exome sequencing data led to the identification of a pathogenic c.1180 C > T variant (NM_198159.3) in the MITF gene, which is likely to be a causative factor for non-syndromic hearing loss in this family. This particular nucleotide substitution leads to the formation of a premature stop codon at amino acid position 394 (p. Arg394Ter, NP_937802.1) of the MITF protein. It is predicted that this will result in a truncated and potentially non-functional protein product. The identified pathogenic variant was detected in a heterozygous state in 13 of the affected individuals, which is consistent with an autosomal dominant inheritance pattern. However, the pathogenic variant was also detected in a homozygous state in 2 individuals. Also, in examining the clinical manifestations of this mutation, no notable differences were observed between homozygous and heterozygous individuals. The c.1180C>T variant in MITF (NM_198159.3), previously reported in ClinVar (Variation ID: 995923) as pathogenic for Waardenburg syndrome type 2A, was identified. Unlike prior reports associating this variant with a broad spectrum of symptoms, including pigmentation abnormalities, our study found it to be linked solely to hearing loss in this population. Notably, no differences in clinical manifestations were observed between homozygous and heterozygous individuals, suggesting population-specific factors may influence the phenotypic expression of this variant.
Correction: IGF1 is Reduced in Pregnancies with Preeclampsia and its Influence on Biological Behavior of Trophoblast Cells.
Qin Y, Meng S, Lyu C … +1 more , Wang S
Biochem Genet · 2025 Nov · PMID 41296144 · Publisher ↗
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Comprehensive Bioinformatics and Functional Analysis Identified MCM5 Facilitates Glioblastoma Progression Through Cell Cycle Regulation.
Ye Y, Song B, Yang W … +5 more , Xie Y, Zhuang D, Ruan J, Ye H, Cheng H
Biochem Genet · 2025 Nov · PMID 41296143 · Publisher ↗
Minichromosome maintenance protein 5 (MCM5) has emerged as a prominent oncogenic across multiple malignancies. However, its role in glioblastoma (GBM) remains unclear. This study investigates the mechanistic role of MCM5...
Minichromosome maintenance protein 5 (MCM5) has emerged as a prominent oncogenic across multiple malignancies. However, its role in glioblastoma (GBM) remains unclear. This study investigates the mechanistic role of MCM5 in GBM pathogenesis. We performed pan-cancer analysis of MCM5 by public datasets (TCGA, GTEx), with particular focus on its expression in GBM, and functional validation by siRNA-mediated knockdown in GBM cell lines (LN18, U87). GO enrichment analysis of MCM5 and its related functional genes was performed using the Metascape database to identify MCM5-related pathways. We subsequently used a variety of experimental methods to thoroughly examine the effect of MCM5 dysfunction on cellular functions, including a subcutaneous hypodermic tumour transplantation model in nude mice, flow cytometry, Transwell assays and wound healing assays. MCM5 exhibited significant overexpression in GBM tissues compared to normal controls. Furthermore, MCM5 expression demonstrated positive correlations with Th2 cells, aCD, and other immune cells. Gene enrichment analysis suggested that MCM5 plays a role in cancer development by regulating deoxyribonucleic acid (DNA) replication. In vitro and in vivo experiments showed that MCM5 enhances GBM cell proliferation, migratory capacity, and cell cycle progression. By bioinformatics analysis and cell experiments, MCM5 is found to promote the progression of GBM by accelerating cell cycle. These findings will provide new clues for the mechanism exploration and prognostic prediction of GBM.
The N6-methyladenosine Modified EphA10 Promotes Prostate Cancer Progression by Activating the ERK/AKT Pathway.
Hu L, Tong J, Tian D … +1 more , Liu Q
Biochem Genet · 2025 Nov · PMID 41296142 · Publisher ↗
Prostate cancer (PCa) is highly aggressive and poses significant threats to health. Investigating the molecular regulatory mechanisms that potentially inhibit tumor progression is essential to identifying valuable target...
Prostate cancer (PCa) is highly aggressive and poses significant threats to health. Investigating the molecular regulatory mechanisms that potentially inhibit tumor progression is essential to identifying valuable target genes for therapeutic intervention. Bioinformatics techniques were employed to explore potential key target genes. siRNA interference was used to construct gene knockdown cell models. Dot blot and MeRIP-qPCR techniques are utilized to investigate the overall N6-methyladenosine (m6A) methylation levels of the target gene. qRT-PCR was used to evaluate the mRNA expression levels of the genes, while Western blotting analysis was performed to detect the protein expression levels of the target genes. The results from bioinformatics, Western blotting and qRT-PCR demonstrate that EphA10 is significantly overexpressed in PCa, highlighting its potential as a target gene for PCa. Mechanistically, EphA10 mRNA undergoes m6A modification mediated by RBM15B, which enhances its stability and expression. YTHDF1 has been identified as an m6A reader for EphA10, promoting its stability and expression in an m6A-dependent manner. Furthermore, the study reveals that m6A-modified EphA10 accelerates PCa cell proliferation, invasion, and migration by activating the ERK/AKT signaling pathway. Our findings suggest that PCa stabilizes the m6A methylation of EphA10, thereby sustaining the activation of the ERK/AKT signaling pathway and accelerating cancer progression. Targeting EphA10, or the m6A methylation "writer" and "reader" proteins involved in its regulation, to inhibit this methylation process could represent a promising therapeutic strategy for PCa.
JHDM1D-AS1 Facilitates Progression of Colorectal Cancer via the miR-193b-3p/HPRT1 Axis.
Li Y, Liu W, Liu C … +2 more , Wang G, Zhou X
Biochem Genet · 2025 Nov · PMID 41296141 · Publisher ↗
Colorectal cancer (CRC) is a critical global health challenge and ranks third among commonly diagnosed malignancies worldwide. As a cancer related long-noncoding RNA (lncRNA), Jumonji C domain containing histone demethyl...
Colorectal cancer (CRC) is a critical global health challenge and ranks third among commonly diagnosed malignancies worldwide. As a cancer related long-noncoding RNA (lncRNA), Jumonji C domain containing histone demethylase 1 homolog D antisense 1 (JHDM1D-AS1) is analyzed to be differentially expressed in CRC samples according to bioinformatics analysis. This study aimed to further explore its effects on CRC cellular process and tumor growth as well as the related mechanisms. Quantitative polymerase chain reaction (RT-qPCR) was utilized to assess expression levels of JHDM1D-AS1 and its downstream molecules in CRC tissues and cells. Functional assays, including colony formation, wound healing, and Transwell assays, were performed to evaluate cellular processes such as proliferation, migration, and invasion. In vivo xenograft and metastasis models were established to examine tumor growth and liver metastasis. The subcellular distribution of JHDM1D-AS1 in CRC cells was measured using fluorescence in situ hybridization (FISH). RNA pulldown and luciferase reporter assays were conducted to confirm molecular interactions. HPRT1 protein expression was quantified using Western blotting. JHDM1D-AS1 is significantly upregulated in CRC cells. Knockdown of JHDM1D-AS1 suppresses CRC cell proliferation, migration, and invasion as well as xenograft tumor growth. JHDM1D-AS1 interacts with miR-193b-3p to regulate HPRT1 expression. MiR-193b-3p targets and downregulates HPRT1. Overexpression of HPRT1 reverses the suppressive effects caused by JHDM1D-AS1 depletion on CRC cell malignancy. In conclusion, JHDM1D-AS1 promotes CRC cell proliferation, metastasis, invasion and tumor development by upregulating HPRT1 expression via miR-193b-3p.
Microsatellite Markers Unveil the Genetic Tapestry of Milkfish Chanos chanos (Fabricius, 1775) in Indian Aquatic Realms.
Jose DM, Divya PR
Biochem Genet · 2025 Nov · PMID 41296140 · Publisher ↗
Chanos chanos (Milkfish) is an ecologically and economically important aquaculture species in the Indo-Pacific, valued for its rapid growth, broad salinity tolerance, and high market demand. Sustainable utilization of th...
Chanos chanos (Milkfish) is an ecologically and economically important aquaculture species in the Indo-Pacific, valued for its rapid growth, broad salinity tolerance, and high market demand. Sustainable utilization of this resource requires a clear understanding of its population genetic structure. In this study, we used 20 microsatellite loci to assess genetic variation across five Indian locations. These markers exhibited high resolution, with a mean polymorphic information content (PIC) value of 0.841, making them highly suitable for population genetic analyses. Analyses revealed high levels of genetic diversity w.r.to parameter like observed and exected heterozygosity (mean H = 0.897; H = 0.867), with an average of 14 alleles per locus. The global F was low but significant (0.008; P = 0.000), indicating weak genetic differentiation. Hierarchical AMOVA, grouping Chilika separately from other populations, showed a slight but significant difference between groups (F = 0.034; P = 0.023), while most genetic variation occurred within populations. These findings highlighted the importance of conserving natural genetic resources while enabling stock-specific management and selective crossbreeding strategies to enhance heterosis, improve aquaculture resilience, and ensure the long-term sustainability of Milkfish farming.
Effects of LncRNA HOXC13-AS on the Prognosis of Non-small Cell Lung Cancer Patients and Its Mechanism of Disease Progression.
You Y, Guan X, Liu Y … +1 more , Yue J
Biochem Genet · 2025 Nov · PMID 41296139 · Publisher ↗
The objective of this research was to explore the impact of HOXC13-AS on the prognosis of NSCLC patients and the mechanism underlying disease progression. The study included 124 NSCLC patients. The expression levels of H...
The objective of this research was to explore the impact of HOXC13-AS on the prognosis of NSCLC patients and the mechanism underlying disease progression. The study included 124 NSCLC patients. The expression levels of HOXC13-AS and miR-218-1-3p in NSCLC tissues and cells were assessed by RT-qPCR. The cumulative survival of NSCLC patients was examined by the Kaplan-Meier method. Cell viability was determined by MTT. Transwell was adopted to evaluate the migration and invasion capabilities of the cells. The interaction between HOXC13-AS and miR-218-1-3p was verified by luciferase reporter assay and RIP assay. Pearson correlation coefficient was utilized to assess the relationship between HOXC13-AS and miR-218-1-3p. HOXC13-AS was elevated in NSCLC tissues and cells, and patients with high HOXC13-AS expression had poorer cumulative survival than the low expression group. Silencing of HOXC13-AS led to a decrease in HOXC13-AS expression and inhibition of cell proliferation, migration and invasion in cells. Experiments confirmed that HOXC13-AS targets miR-218-1-3p. miR-218-1-3p was downregulated in NSCLC tissues and cells, and HOXC13-AS was negatively correlated with miR-218-1-3p. After silencing HOXC13-AS, further inhibition of miR-218-1-3p led to a decrease in its levels and enhanced cell proliferation, migration, and invasion. In NSCLC patients, HOXC13-AS is aberrant expression and closely associated with poor prognosis. Inhibition of miR-218-1-3p expression partially reverses the inhibitory effects of HOXC13-AS silencing on NSCLC cells. This suggests that HOXC13-AS could serve as a promising biomarker for NSCLC, providing new insights into NSCLC progression.
Methodology for the Analysis of Odorant-Binding Proteins in Asiatic Genetic Groups of Bemisia tabaci.
Gouda MNR, Subramanian S
Biochem Genet · 2025 Nov · PMID 41296138 · Publisher ↗
Insects rely heavily on their olfactory system for crucial behaviours like finding mates, locating food, and avoiding predators. Odorant binding proteins (OBPs) bind to odorant molecules, facilitating their transport to...
Insects rely heavily on their olfactory system for crucial behaviours like finding mates, locating food, and avoiding predators. Odorant binding proteins (OBPs) bind to odorant molecules, facilitating their transport to olfactory receptors. Understanding OBP diversity and the genomic landscape is vital for elucidating insect olfaction. Bemisia tabaci, a global invasive pest with significant economic impact, has limited OBP diversity studies across its genetic groups. This research investigates OBPs in B. tabaci Asiatic groups, a major invasive genetic group in Asia, to enhance our knowledge of their olfactory mechanisms and inform targeted pest control strategies. A computational pipeline identified OBPs in B. tabaci Asiatic groups using TBLASTN analysis of annotated genomes and whole-genome data. Unique OBP sequences were verified with BLASTX. Bioinformatics tools analysed gene structure, domain prediction, chromosomal localization, scaffold-wise arrangement, and protein structure. Phylogenetic analyses characterised OBPs and explored evolutionary relationships. We identified 9-10 OBPs in B. tabaci Asiatic groups, expanding our knowledge beyond previously studied genetic groups. Comparative analyses with other Hemipteran species showed similarities and differences in OBP diversity. Functional domain analysis highlighted conserved domains associated with odorant binding and membrane interactions. Variations in signal peptide presence suggested differences in protein stability and ligand-binding capabilities. Genomic organisation analysis revealed non-random OBP gene clustering on specific chromosomes, indicating potential co-regulation and functional relationships. The findings enhance understanding of B. tabaci olfaction and provide insights for targeted pest control strategies.
Predictive Value of C-Reactive Protein-Albumin-Lymphocyte Index for Multiple Organ Failure Syndrome in Elderly Patients with Sepsis.
Fan Z, Zhang Y, Liu S … +2 more , Xu H, Guo Y
Biochem Genet · 2025 Nov · PMID 41296137 · Publisher ↗
This study evaluates the C-reactive protein-albumin-lymphocyte (CALLY) index for predicting multiple organ failure syndrome (MOFS) in elderly with sepsis (SP) through a retrospective analysis of 209 cases stratified by s...
This study evaluates the C-reactive protein-albumin-lymphocyte (CALLY) index for predicting multiple organ failure syndrome (MOFS) in elderly with sepsis (SP) through a retrospective analysis of 209 cases stratified by severity into SP, severe SP (SSP), and septic shock (SPS) groups. Patients were further categorized into MOFS and N-MOFS groups according to 30-day ICU outcomes. Correlations of CALLY index with APACHE II and SOFA scores were assessed using Spearman's correlation analysis, while predictive utility was evaluated via ROC and Kaplan-Meier curves and Cox regression. Results demonstrated a progressive decline in CALLY index with worsening severity (SPS < SSP < SP; P < 0.001), alongside negative correlations with APACHE II and SOFA scores (P < 0.001). Patients who developed MOFS exhibited a significantly lower CALLY index than their N-MOFS counterparts (P < 0.05). The index achieved superior MOFS prediction (AUC = 0.892) compared to APACHE II (AUC = 0.772; P < 0.001) and SOFA (AUC = 0.815; P = 0.042), with low-CALLY patients showing higher cumulative MOFS incidence (P < 0.001). Multivariate analysis confirmed elevated SOFA as an independent risk factor for MOFS, while higher CALLY index conferred protective effects, establishing this novel index as a robust predictor of MOFS that inversely correlates with SP severity in elderly.
The Impact of the FXR1-FUBP1 Axis on Chemotherapy Resistance in LUSC Cells.
Liang R, Li Y, Chen J … +1 more , Deng H
Biochem Genet · 2025 Nov · PMID 41273664 · Publisher ↗
This study investigates the role of the transcription factor FUBP1 in mediating chemotherapy resistance and immune evasion in lung squamous cell carcinoma (LUSC), and its regulation by Fragile X mental retardation syndro...
This study investigates the role of the transcription factor FUBP1 in mediating chemotherapy resistance and immune evasion in lung squamous cell carcinoma (LUSC), and its regulation by Fragile X mental retardation syndrome-related protein 1 (FXR1). Bioinformatics analysis identified potential targets in LUSC. Paclitaxel-resistant LUSC cell lines (H520 R and H226 R) were established, with chemotherapy resistance assessed using Cell Counting Kit-8 (CCK-8) assays. Lentiviral infection was used to achieve FXR1 or Far upstream element-binding protein 1 (FUBP1) knockdown, or FUBP1 overexpression. Molecular analyses included RT-qPCR, Western blot, RNA immunoprecipitation, and actinomycin D chase assays. Chemosensitivity was evaluated using CCK-8 and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays, while phosphorylated H2A histone family member X (γ-H2AX) and Programmed death-ligand 1 (PD-L1) expression levels were detected via Western blot. Immune function was examined using CD8⁺ T cell co-cultures with lactate dehydrogenase cytotoxicity assays. In vivo validation was performed using xenograft models treated with paclitaxel. FUBP1 was significantly upregulated in LUSC tumors and chemoresistant cells. Its depletion enhanced chemosensitivity, evidenced by reduced cell viability, enhanced apoptosis, and elevated γ-H2AX expression. FUBP1 knockdown also lowered PD-L1 expression and augmented CD8+ T cell cytotoxicity. FXR1 knockdown decreased FUBP1 expression by reducing its mRNA stability, thereby increasing chemosensitivity and attenuating immune evasion. In vivo, FXR1 silencing suppressed tumor growth, reduced PD-L1 expression, and increased granzyme B, and perforin levels, effects that were reversed by FUBP1 overexpression. The FXR1-FUBP1 axis critically mediates chemoresistance and immune evasion in LUSC, providing novel therapeutic targets for overcoming treatment resistance.
Urinary DNA Methylation Profiling Improves Discrimination of Prostate Cancer Across PSA-Defined Risk Strata.
Zhu W, Qian Y, Zhao X … +14 more , Fang Z, Luo Z, Xie W, Cao Y, Chen W, Fu H, Peng J, Zhang L, Li J, Lei S, Jin J, Gong Z, Zhang D, He Y
Biochem Genet · 2025 Nov · PMID 41247441 · Publisher ↗
Prostate-specific antigen (PSA) testing lacks specificity due to benign conditions. This study assessed whether integrating DNA methylation signatures with PSA metrics improves discrimination of prostate cancer (PCa) fro...
Prostate-specific antigen (PSA) testing lacks specificity due to benign conditions. This study assessed whether integrating DNA methylation signatures with PSA metrics improves discrimination of prostate cancer (PCa) from non-PCa cases. Targeted bisulfite sequencing of 74 CpG sites in 9 genes was performed on urine sediment from 194 patients (89 PCa, 105 non-PCa). Patients were stratified by total PSA (tPSA) and free-to-total PSA ratio (%fPSA) into risk groups. Random forest identified discriminatory methylation markers, and support vector machine (SVM), k-nearest neighbor (KNN), and Bayesian models were constructed and validated. PSA-based stratification alone could not reliably distinguish PCa from non-PCa, with 26.80% of patients falling into a diagnostic "gray zone". Twenty CpG sites showed significant differential methylation (p < 0.01). In addition, several CpG loci exhibited methylation differences across PSA risk groups. Models based on random forest-selected markers achieved strong diagnostic performance, with KNN yielding the highest accuracy (AUC > 0.95, 100% specificity), and consistently high sensitivity (> 80%), maintaining strong discriminative power even in PSA "gray-zone" cases. Urine-based DNA methylation profiling enhances the diagnostic accuracy of PCa beyond PSA testing, particularly in cases within the PSA gray zone. Validation in larger independent cohorts is warranted to establish its clinical utility.
Unveiling Dynamic Defense Pathways: Transcriptome Analysis of Phenylpropanoids and (Iso)flavonoids in Cowpea Leaves Post-CABMV Inoculation.
de Andrade Luz G, da Costa Gomes MF, Ferreira-Neto JRC … +4 more , da Costa AF, Sperandio MVL, Benko-Iseppon AM, Kido EA
Biochem Genet · 2025 Nov · PMID 41240170 · Publisher ↗
Plants exhibit sophisticated defense mechanisms orchestrated by intricate molecular responses to biotic stresses. Here, we investigate the transcriptional dynamics of the CABMV-resistant cowpea line IT85F-2687 following...
Plants exhibit sophisticated defense mechanisms orchestrated by intricate molecular responses to biotic stresses. Here, we investigate the transcriptional dynamics of the CABMV-resistant cowpea line IT85F-2687 following mechanical injury and Cowpea aphid-borne mosaic virus (CABMV) inoculation. Transcriptome analysis revealed rapid up-regulation of genes associated with the shikimate pathway, notably DAHPS, ADT-PDT, and ADH, within one hour post-inoculation. Subsequent activation of phenylpropanoid and isoflavonoid pathways underscored the cowpea's adaptive responses, probably enhancing the synthesis of secondary metabolites crucial for defense. Transcripts encoding enzymes such as PAL, 4CL, and CHS were prominently upregulated, potentially directing metabolic flux towards lignin, flavonoid, and phytoalexin biosynthesis. The study also identified enrichment of transcription factor families (WRKY, MYB, bHLH) implicated in stress responses and secondary metabolism regulation. Comparative genomics highlighted conservation of orthologs among legume species, suggesting evolutionary significance and potential utility for breeding resilient cultivars. These findings advance our understanding of plant-pathogen interactions and propose strategies for developing cowpea varieties with enhanced resistance to biotic stresses, contributing to sustainable agriculture.
Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p.
Liu X, Shi Y, Huang L … +7 more , Chen H, Fan R, Zhang H, Li Q, Yan N, He M, Yang Y
Biochem Genet · 2025 Nov · PMID 41240169 · Publisher ↗
Acute lung injury (ALI) is a severe respiratory syndrome for which there is still a lack of effective treatment. Salvianolic acid A (Sal A) is a bioactive polyphenol extracted from Salvia miltiorrhiza Bunge, which has an...
Acute lung injury (ALI) is a severe respiratory syndrome for which there is still a lack of effective treatment. Salvianolic acid A (Sal A) is a bioactive polyphenol extracted from Salvia miltiorrhiza Bunge, which has anti-inflammatory and antioxidant effects, but its role in ALI is unclear. We injected 50 µL LPS into the trachea of mice, and treated MLE-12 cells with 1 µg/mL LPS to construct ALI mouse and cell model. The levels of genes and proteins was identified using RT‒qPCR, western blot and immunofluorescence. The damage of MLE-12 cells and mouse lung tissue was evaluated by CCK-8, ELISA, TUNEL and HE staining. Sal A treatment can significantly inhibit LPS-induced inflammation and apoptosis, and then inhibit MLE-12 cell damage and ALI progression. From a mechanistic standpoint, Sal A promotes the expression of LC3 II/I and Beclin1, suppresses p62 expression, increases cell autophagy, and suppresses LPS-induced inflammatory cytokines IL-6, IL-1β, and TNF-α expression, ultimately reducing LPS-induced inflammation in lung epithelial cells and alleviating ALI progression. The main function of Sal A is to achieve this by inhibiting the expression of miR-217-5p and thereby promoting the expression of FOXO1. Our research results may provide a new target for the treatment of ALI with Sal A.
Investigation of Genetic Polymorphisms in Inducible Nitric Oxide Synthase and Suppressor of Cytokine Signaling Genes and Pain After Root Canal Treatment.
Nascimento WM, da Silva EAB, Meyfarth SRS … +9 more , da Silva Guimarães L, Limoeiro AG, Ribeiro HG, Küchler EC, Baratto-Filho F, Silva-Sousa AC, Sousa-Neto MD, Antunes LAA, Antunes LS
Biochem Genet · 2025 Nov · PMID 41240168 · Publisher ↗
Pain following endodontic treatment is a common complication potentially linked with genetic polymorphisms that modulate pain biomarkers. Hence, this study aimed to explore the association between pain experienced after...
Pain following endodontic treatment is a common complication potentially linked with genetic polymorphisms that modulate pain biomarkers. Hence, this study aimed to explore the association between pain experienced after endodontic treatment and genetic polymorphisms in the genes encoding inducible nitric oxide synthase (NOS2), and suppressor of cytokine signaling (SOCS1). The study involved 108 participants with single-rooted teeth, single canals, and necrotic pulp related to asymptomatic apical periodontitis. All endodontic treatments were executed in a single session. Pain and tenderness levels were measured using a visual analog scale (VAS) on the 1st, 2nd, 3rd, 4th, 5th, 6th, 7th, 14th, and 30th day post-treatment. Genomic deoxyribonucleic acid (DNA) was extracted from saliva cells and the genetic polymorphisms rs2779249, rs2297518, rs243327 and rs33977706 were genotyped using real-time polymerase chain reaction. Genotype distribution was assessed using univariate and multivariate Poisson regressions through generalized estimating equations (GEE) and categorized based on the presence or absence of pain and tenderness, and the significance threshold was set at p < 0.05. The genetic polymorphism rs2297518 in the NOS2 gene was associated with pain in the recessive model (p = 0.019) and to tenderness in both the codominant (p = 0.008) and recessive (p < 0.001) models. The genetic polymorphisms rs2779249 in NOS2 and rs243327 and rs33977706 in SOCS1 showed no association with pain or tenderness (p > 0.05). In conclusion, the genetic polymorphism rs2297518 in the NOS2 gene was associated with pain after root canal treatment. These findings contribute to a better understanding of the genetic factors influencing postoperative pain in endodontics, which may help in developing personalized pain management strategies and improving patient care.
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