Human Cell[JOURNAL]
Sun
200 papers
Establishment and characterization of patient-derived tongue squamous cell carcinoma cell lines.
Joshi P, Bane S, Chaturvedi P … +2 more , Gera P, Waghmare SK
Hum Cell · 2025 May · PMID 40394426 · Full text
Oral squamous cell carcinoma (OSCC) is a common carcinoma in Indian population, wherein one-third of global OSCC cases are from India. The five-year survival rate is poor due to late diagnosis. Oral tongue squamous cell...
Oral squamous cell carcinoma (OSCC) is a common carcinoma in Indian population, wherein one-third of global OSCC cases are from India. The five-year survival rate is poor due to late diagnosis. Oral tongue squamous cell carcinoma (OTSCC) is the second-most common OSCC. An in vitro cell line model is a valuable tool to get a deeper understanding of the molecular mechanisms involved in therapy resistance and disease progression. We report establishment of three OTSCC cell lines from advanced stage treatment naïve Indian patient samples, such as ACOTSC120, ACOSTC132, and ACOTSC140. All three OTSCC cell lines showed epithelial morphology, which was confirmed by Keratin-14 staining. The cell lines showed in vitro spheroid-forming and in vivo tumorigenic potential. The STR of the cell lines ensured their human origin and novelty when compared to DSMZ cell line database. The karyotype of the cell lines showed aneuploidy and further confirmed their human origin. These cell lines showed the presence of cancer stem cell (CSCs) population, i.e., the ALDH/CD44 population. These cell lines thus provide a model to help understand the biology of disease and its progression.
The role of microglia in the development of diabetic retinopathy and its potential clinical application.
Lu T, Shang J, Pu S … +3 more , Xu Y, Sun X, Gao X
Hum Cell · 2025 May · PMID 40392429 · Publisher ↗
Lately, research on the function of microglia in diabetic retinopathy (DR) is becoming increasingly focused. Microglia are immune cells that dwell in the central nervous system and are crucial to the pathophysiology of D...
Lately, research on the function of microglia in diabetic retinopathy (DR) is becoming increasingly focused. Microglia are immune cells that dwell in the central nervous system and are crucial to the pathophysiology of DR. According to studies, a hyperglycemic environment can activate microglia, bringing them out of a resting state to an active state. This allows them to release a variety of inflammatory factors and chemokines, which can then cause retinal inflammatory reactions. When it comes to angiogenesis in DR, activated microglia release a variety of angiogenic substances, such as vascular endothelial growth factor (VEGF), to create aberrant new blood vessels. Moreover, microglia contribute to the retina's oxidative stress process by generating and releasing reactive oxygen and nitrogen-free radicals, which exacerbates retinal damage. Researchers have proposed a variety of strategies for the activation of microglia and the inflammatory response it triggers. By inhibiting the excessive activation of microglia and reducing the release of inflammatory factors, the inflammatory response and damage to the retina can be alleviated. Drugs that interfere with retinal microglia can also be used to regulate vascular damage and inhibit the formation of new blood vessels. In addition, antioxidants are used to remove reactive oxygen and free radicals, reduce oxidative stress levels, and protect retinal cells. These therapeutic strategies aim to achieve the purpose of treating DR by regulating the function of microglia. Thus, we highlight the possibility that therapy aimed at microglia could offer fresh ideas for treating DR.
Sunitinib-resistant renal cell carcinoma cell-derived exosomes promote facilitation of tumor progression via secretion of the lncRNA SNHG16.
Saimaiti W, Ma J, Dilimulati P … +1 more , Wang Y
Hum Cell · 2025 May · PMID 40358820 · Publisher ↗
Renal cell carcinoma (RCC) is one of the most common tumors of high malignancy in the urological system. Sunitinib is commonly used to treat RCC, while drug resistance severely limited the therapeutic efficacy. Tumor-der...
Renal cell carcinoma (RCC) is one of the most common tumors of high malignancy in the urological system. Sunitinib is commonly used to treat RCC, while drug resistance severely limited the therapeutic efficacy. Tumor-derived exosomes play important roles in facilitating cancer development. However, the role of drug-resistant tumor-derived exosomes in tumorigenesis and resistance of RCC has not been elucidated. Here we isolated sunitinib-sensitive/resistant RCC cells-derived exosomes, characterized by transmission electron microscopy (TEM) and western blot. Furthermore, co-culture experiments were performed and we found that sunitinib-resistant RCC cells-derived exosomes (R-exos) promoted cell proliferation and upregulated proliferation-related genes cyclin D1 (CCND1) and proliferating cell nuclear antigen (PCNA) expression, and inhibited apoptosis and the expression of Bax and Caspase-3 of sunitinib-resistant RCC (RCC/R) cells by delivering lncRNA small nuclear RNA host gene 16 (SNHG16). In resistant cell-derived xenograft (CDX-R) models, R-exos induced tumor growth in vivo, while knockdown of SNHG16 effectively diminished the tumorigenesis of RCC. Moreover, SNHG16 positively regulated the expression of trophinin associated protein (TROAP) by sponging miR-106a-5p in RCC cells, whereas inhibition of miR-106a-5p or overexpression of TROAP greatly reversed the suppression of tumorigenesis and sunitinib resistant by silencing SNHG16. R-exos lncRNA SNHG16 promoted sunitinib resistant and malignant progress by regulating the miR-106a-5p/TROAP axis, and targeting SNHG16/miR-106a-5p/TROAP axis may be a novel therapeutic approach for sunitinib-treated patients of RCC.
Advanced glycation end products alter the structural integrity, increase the permeability and transform the biocompatibility of collagen within the peritoneal membrane.
Fukuda M, Chiwata Y, Narita T … +9 more , Yoshihara M, Morimoto H, Takamori A, Shibuki S, Hinami R, Ishibashi A, Nagashima A, Miyazono M, Aoki S
Hum Cell · 2025 May · PMID 40353921 · Publisher ↗
In patients undergoing long-term peritoneal dialysis, the peritoneal accumulation of advanced glycation end-products (AGEs) due to the Maillard reaction has long been acknowledged as problematic, although the underlying...
In patients undergoing long-term peritoneal dialysis, the peritoneal accumulation of advanced glycation end-products (AGEs) due to the Maillard reaction has long been acknowledged as problematic, although the underlying mechanisms remain insufficiently understood. Recognizing collagen as both a principal substrate for AGEs deposition and a vital cellular scaffold, we developed an innovative procedure that induces the Maillard reaction in collagen at near-physiological temperatures, enabling systematic evaluations of its structural and functional modifications. Our findings reveal that Maillard reaction-treated collagen exhibits markedly increased permeability to small- and medium-sized molecules. Furthermore, this denatured collagen diminishes the proliferative capacity of adherent mesothelial cells, implicating glycation-induced alterations in collagen in the progressive deterioration of peritoneal membrane function during extended dialysis. By illuminating previously uncharacterized morphological and functional shifts in collagen triggered by the Maillard reaction, our model provides critical insights that will enhance the safety of peritoneal dialysis and inform the development of novel therapeutic strategies.
Establishment and characterization of Cri Du Chat neuronal stem cells: a novel promising resource to study the syndrome.
Piovani G, Ferraro RM, Giliani SC
Hum Cell · 2025 May · PMID 40343585 · Full text
The Cri Du Chat (CdC) Syndrome is a rare chromosome disease condition resulting from variable size deletion occurring on the short arm of one of the chromosomes 5. This disorder, which affects one in 50,000 births, is re...
The Cri Du Chat (CdC) Syndrome is a rare chromosome disease condition resulting from variable size deletion occurring on the short arm of one of the chromosomes 5. This disorder, which affects one in 50,000 births, is responsible for developmental retardation, the mechanism of which has remained unexplained. TERT, SEMA5 A, CTNND2, TPPP, mapped in chromosome 5 short arm, are known to be expressed in the brain, and to play a role in the development of the nervous system, oligodentrocytes and in the regulation of glutamatergic and dopaminergic synaptic transmission. It is critical to understand how their haploinsufficiency might affect the development and presentation of the disease. In the absence of an animal model and of significant accessible, human tissue, human pluripotent stem cells (iPSC) directly reprogrammed from patient somatic cells open a new area of disease modeling as they can virtually be differentiated into any cell type. Our study reports, for the first time, the generation of neuronal stem cells (NSCs) from CdC-iPSCs line and in addition, subsequent differentiation into a heterogeneous population of neurons. Gene expression of the mentioned and single copy deleted genes was also evaluated by comparing their expression level in iPSC, NSCs and neuron lines. The present research represents the first and the most innovative approach, to create an in vitro CdC neuronal model to have a new translational framework to study the pathologic processes.
Screening of pivotal oncogenes modulated by DNA methylation in hepatocellular carcinoma and identification of atractylenolide I as an anti-cancer drug.
Zhi Y, Qiaoyun T
Hum Cell · 2025 May · PMID 40325252 · Publisher ↗
This study was performed to identify crucial oncogenes modulated by DNA methylation in hepatocellular carcinoma (HCC) and look for new drugs for HCC treatment. The data of TCGA-LIHC cohort were obtained from UCSC databas...
This study was performed to identify crucial oncogenes modulated by DNA methylation in hepatocellular carcinoma (HCC) and look for new drugs for HCC treatment. The data of TCGA-LIHC cohort were obtained from UCSC database. Weighted gene co-expression network analysis and multiple machine learning algorithms were applied to screen the crucial prognosis-related genes in HCC. Then these genes were further screened by DNA methylation status. Ten-eleven translocation 1 (TET1) was overexpressed in HCC cell lines, and its biological functions and regulatory effects on the oncogenes were explored by qPCR, methylation-specific polymerase chain reaction, cell viability assay, Western blot, etc. Molecular docking was applied to evaluate the binding affinity between atractylenolide I (AT-I) and TET1, and the tumor-suppressive functions of AT-I were examined with both in vitro and in vivo models. In this work, 12 crucial genes related to HCC prognosis were obtained, among which six genes were with differential methylation status in HCC tissues, including AKR1B10, ALPK3, NQO1, NT5DC2, SFN, and SPP1. The expression levels of ALPK3 and NT5DC2 were positively regulated by TET1, the crucial mediator of demethylation. TET1 overexpression increased the viability and stemness of HCC cells. AT-I had good binding affinity with TET1, and repressed its activity. AT-I promoted the methylation of ALPK3 and NT5DC2 promoter regions, and reduced their expression, and repressed the growth of HCC cells. In summary, DNA methylation contributes to HCC progression, and AT-I represses the malignancy of HCC cells by inhibiting TET1-mediated abnormal DNA demethylation.
Deficiency of synaptotagmin-1 aggravates pressure overload-induced cardiac hypertrophy and dysfunction via the p38 MAPK signaling pathway in mice.
Shen J, Miao J, Wu L … +4 more , Wang D, Li G, Wang H, Cao J
Hum Cell · 2025 Apr · PMID 40279007 · Full text
Cardiac hypertrophy is a major risk factor for heart failure and sudden cardiac death, but its molecular mechanisms have not been well clarified. Synaptotagmin-1 (SYT1) is an important regulator of exocytosis and apoptos...
Cardiac hypertrophy is a major risk factor for heart failure and sudden cardiac death, but its molecular mechanisms have not been well clarified. Synaptotagmin-1 (SYT1) is an important regulator of exocytosis and apoptosis and has been found expressed in the myocardium, while its functions in heart diseases have rarely been studied. Here, we investigated the role and mechanism of SYT1 in pressure overload-induced cardiac hypertrophy. Transverse aortic constriction (TAC) surgeries were performed to induce cardiac hypertrophy in global Syt1 knockout (Syt1) mice and C57BL/6J wild-type (WT) littermates in vivo, with respective sham mice as negative controls. Cardiomyocyte hypertrophy was induced by angiotensin II (Ang II) in H9C2 cells in vitro. The results showed that SYT1 expression was significantly upregulated in WT-TAC mice and in Ang II-treated H9C2 cells. Blocking angiotensin receptor by losartan decreased SYT1 expression in Ang II-treated H9C2 cells. Syt1 mice showed significantly exacerbated cardiac hypertrophy, dysfunction, fibrosis, apoptosis and phosphorylation of myocardial p38 MAPK in response to TAC compared to WT mice. Knocking down SYT1 using siRNA in H9C2 cells aggravated Ang II-induced cell hypertrophy and apoptosis, and also enhanced p38 MAPK phosphorylation. Inhibition of p38 MAPK by SB203580 significantly alleviated the hypertrophy and apoptosis in Ang II-treated H9C2 cells. We conclude that deficiency of SYT1 aggravates pressure overload-induced cardiac hypertrophy via the p38 MAPK signaling pathway. The study elucidates a novel role of SYT1 in cardiac remodeling.
Generation of human induced pluripotent stem cell lines derived from a patient carrying an intragenic deletion in the NFIA gene.
Zhou N, Zhang S, Wang C … +3 more , Zheng B, Zhang A, Zhou W
Hum Cell · 2025 Apr · PMID 40266456 · Publisher ↗
Brain malformations with or without urinary tract defects (BRMUTD) are caused by heterozygous variants in the NFIA gene. BRMUTD is a neurodevelopmental disorder characterized by hypoplasia or absence of the corpus callos...
Brain malformations with or without urinary tract defects (BRMUTD) are caused by heterozygous variants in the NFIA gene. BRMUTD is a neurodevelopmental disorder characterized by hypoplasia or absence of the corpus callosum, hydrocephalus or ventriculomegaly, and developmental delay, which may or may not be accompanied by urinary tract defects. Here, we report the successful generation of induced pluripotent stem cells (hiPSCs) from a 3-year-old male BRMUTD patient using Sendai virus-based non-integrating reprogramming technology. This patient-derived cell line harbors an intragenic deletion within the NFIA gene (NC_000001.10: g.61650967_61842967del [GRCh37]), which is associated with a significant reduction in NFIA expression. This cell line maintains a normal karyotype, expresses pluripotency markers, and can differentiate into three germ layers. The established hiPSCs line will provide an in vitro model for studying pathological mechanisms and potential therapies of NFIA-related neurodevelopmental disorder.
Retraction Note: RCC2 contributes to tumor invasion and chemoresistance to cisplatin in hepatocellular carcinoma.
Chen Q, Jiang P, Jia B … +2 more , Liu Y, Zhang Z
Hum Cell · 2025 Apr · PMID 40261526 · Publisher ↗
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Establishment and characterization of NCC-PS2-C1: a novel cell line of high-grade pleomorphic spindle cell sarcoma, most consistent with myxofibrosarcoma.
Iwata S, Noguchi R, Osaki J … +8 more , Adachi Y, Shiota Y, Osaki S, Nishino S, Yoshida A, Ohtori S, Kawai A, Kondo T
Hum Cell · 2025 Apr · PMID 40253665 · Publisher ↗
Pleomorphic sarcoma (PS) is a heterogeneous group of malignant mesenchymal tumors that lack specific histological differentiation. PS is characterized by genetic instability and diversity and unique histological features...
Pleomorphic sarcoma (PS) is a heterogeneous group of malignant mesenchymal tumors that lack specific histological differentiation. PS is characterized by genetic instability and diversity and unique histological features such as pronounced morphologic pleomorphism. PS is one of the most common soft tissue sarcomas. Complete surgical resection remains the only curative treatment and is often combined with neoadjuvant radiotherapy. Effective systemic chemotherapy is yet to be established, and PS frequently recurs locally and metastasizes to the lungs. Patient-derived cancer cell lines are invaluable tools for basic and preclinical research for developing novel chemotherapies. Herein, we report a high-grade pleomorphic spindle cell sarcoma, most consistent with myxofibrosarcoma cell line, NCC-PS2-C1, which was derived from a primary tumor specimen. NCC-PS2-C1 cells exhibited a range of copy number alterations. This cell line demonstrated consistent proliferation, spheroid formation, and invasive capabilities in vitro. Drug screening using NCC-PS2-C1 cells revealed that cobimetinib, crenolanib, and ixazomib were effective against PS. In conclusion, we established NCC-PS2-C1 cells from primary tumors of PS. This cell line is a valuable resource for developing novel chemotherapies.
Hyaluronic acid-modified milk exosomes carrying ZNF516 inhibit ABCC5 and contribute to pemetrexed sensitivity in lung adenocarcinoma.
Li H, Sun Y, Wang J … +4 more , Wang Z, Wu L, Lei J, Gao Y
Hum Cell · 2025 Apr · PMID 40253507 · Publisher ↗
Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Milk-derived exosomes (mEXOs) have critical roles in cancer treatment. This paper explores the effects of hyaluronic acid (HA)-modified mEXOs (HA-mEXO...
Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Milk-derived exosomes (mEXOs) have critical roles in cancer treatment. This paper explores the effects of hyaluronic acid (HA)-modified mEXOs (HA-mEXOs) in LUAD. HA-mEXOs were isolated and prepared, and PMX-resistant cells were developed. CCK-8, colony formation, Transwell, flow apoptosis, xenograft tumor assay, immunohistochemistry, and TUNEL experiments were conducted to explore the impact of mEXOs and HA-mEXOs on malignant behaviors and PMX sensitivity. The role of ZNF516 and ABCC5 on malignant behaviors and PMX sensitivity was investigated by shRNA lentiviral infection. HA modification increased the uptake and affinity of LUAD cells for mEXOs. mEXOs induced PMX-resistant LUAD cell sensitivity and inhibited their malignant behaviors. mEXOs enhanced PMX sensitivity and inhibited tumor growth. HA-mEXOs had superior effects to mEXOs. ZNF516 was lowered in LUAD-resistant cells and upregulated by mEXOs. ZNF516 bound to the ABCC5 promoter and repressed its transcriptional activation. The combined knockdown of ZNF516 reversed the antitumor benefits of mEXOs. HA-mEXOs-carrying ZNF516 enhance ZNF516 levels in LUAD/PMX cells and repress ABCC5, which in turn induces cell sensitivity to PMX and inhibits LUAD progression.
LncRNA OLMALINC promotes osteosarcoma progression through USP1-mediated autophagy suppression.
Li J, Yu B, Xue Z … +6 more , Liang Y, Chen S, Gui T, Liu Z, Zhang L, Peng R
Hum Cell · 2025 Apr · PMID 40249458 · Publisher ↗
Osteosarcoma (OS) remains a challenging malignancy with poor prognosis, especially in metastatic or recurrent cases. Despite progress, the molecular mechanisms driving OS, particularly the regulation of autophagy, are no...
Osteosarcoma (OS) remains a challenging malignancy with poor prognosis, especially in metastatic or recurrent cases. Despite progress, the molecular mechanisms driving OS, particularly the regulation of autophagy, are not fully understood. Here, through integrated analysis of single-cell and transcriptomic data, we identify a novel long non-coding RNA (lncRNA), OLMALINC, as a critical autophagy regulator in OS. OLMALINC is significantly upregulated in OS tissues, with its expression correlating to poor clinical outcomes. Functional studies show that altering OLMALINC expression impacts OS cell progression and autophagy. Mechanistically, transcriptome analysis and RNA immunoprecipitation reveal Ubiquitin-Specific Peptidase 1 (USP1) as a direct downstream target of OLMALINC. The OLMALINC-USP1 axis inhibits autophagy and activates the hypoxia-inducible factor 1 (HIF-1α) pathway, promoting OS progression. Therapeutically, combining the USP1 inhibitor ML-323 with doxorubicin demonstrated synergistic anti-tumor effects in vitro and in vivo, enhancing autophagy and apoptosis while inhibiting tumor growth. These findings uncover a novel OLMALINC-USP1-HIF-1α axis in OS progression and highlight the potential of combining autophagy modulation with chemotherapy for improved therapeutic outcomes.
Clinical characteristics and induced pluripotent stem cells (iPSCs) disease model of Harel-Yoon syndrome caused by compound heterozygous ATAD3A variants.
Jiang Z, Chen H, Zhang X … +9 more , Jiang X, Tong Z, Ye J, Shi S, Shi X, Li F, Shao W, Shu Q, Yu L
Hum Cell · 2025 Apr · PMID 40246775 · Publisher ↗
ATPase family AAA-domain-containing protein 3 A (ATAD3A) is enriched on the mitochondrial membrane and is essential to the maintenance of mitochondrial structure and function. Variants of the ATAD3A gene can lead to Hare...
ATPase family AAA-domain-containing protein 3 A (ATAD3A) is enriched on the mitochondrial membrane and is essential to the maintenance of mitochondrial structure and function. Variants of the ATAD3A gene can lead to Harel-Yoon syndrome (HAYOS), a developmental defect in neurological, cardiovascular, and other systems. This study aims to develop induced pluripotent stem cells (iPSCs) from the somatic cells of a patient (ZJUCHYLi001-A) and a negative control (ZJUCHYLi002-A) as effective tools for further investigations into the etiology of ATAD3A variant-related disease. We described and analyzed the clinical manifestations of the proband and her family members. Somatic cells from the proband and a negative control were collected and reprogrammed into iPSCs. Furthermore, we measured the ATAD3A expression levels in the iPSCs to confirm the validity of these cell lines. The proband and her elder sister were both critically ill and harbored compound heterozygous ATAD3A variants (F459S/T498 Nfs* 13). Their parents were carriers of these variants without any clinical manifestations. Both variants are located on the ATPase domain of the ATAD3A protein. Cell lines ZJUCHYLi001-A and ZJUCHYLi002-A presented typical features of pluripotent stem cells. The ATAD3A expression levels of ZJUCHYLi001-A were significantly reduced compared with ZJUCHYLi002-A. This study generated iPSCs from a patient with compound heterozygous variants of ATAD3A and a negative control as valuable tools for clarifying the molecular mechanisms underlying ATAD3A variant-related diseases.
The role of MICAL2 in cancer progression: mechanisms, challenges, and therapeutic potential.
Wang R, Hou Z, Gao X … +3 more , Wu B, Hu H, Wu H
Hum Cell · 2025 Apr · PMID 40240704 · Publisher ↗
Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attracti...
Cancer is the greatest threat to public health worldwide and a major cause of human death. Compared with conventional chemotherapy, agents targeting key oncogenic drivers and signaling mechanisms are becoming an attractive treatment strategy. Molecule interacting with CasL 2 (MICAL2) is a flavin protein monooxygenase family protein that interacts with CasL2 and is involved in cytoskeletal redox regulation, axon-directed regulation, cell transport, and apoptosis. MICAL2 induces F-actin depolymerization through REDOX modification, thereby promoting the expression of epithelial-mesenchymal transition (EMT)-related proteins and inducing cancer cell invasion and proliferation. Mechanistically, MICAL2 induces EMT by regulating the serum response factor (SRF)/myocardin-related transcription factor A (MRTF-A) signaling pathway, and the semaphorin/plexin pathway and inducing reactive oxygen species (ROS) production. Recent studies have shown that MICAL2 is highly expressed in tumors, accelerates tumor progression, and is a novel tumor-promoting factor. This article summarizes recent research findings to review the biological functions of MICAL2, the potential mechanisms related to cancer progression, and discusses the challenges and prospects in this area, providing a new theoretical basis for clinical molecular targeted therapy for cancer.
SIX1 enhances aerobic glycolysis and progression in cervical cancer through ENO1.
Liu X, Ren H, Wang A … +7 more , Liang Z, Min S, Yao S, Wan S, Gao Y, Wang H, Cai H
Hum Cell · 2025 Apr · PMID 40234326 · Publisher ↗
Cervical cancer is a significant threat to women's health, and its incidence in China has been increasing in recent years. Treating advanced and recurrent cervical cancer has become increasingly challenging, highlighting...
Cervical cancer is a significant threat to women's health, and its incidence in China has been increasing in recent years. Treating advanced and recurrent cervical cancer has become increasingly challenging, highlighting the urgent need to identify new therapeutic targets for this disease. SIX1 is associated with cell proliferation, metastasis, and chemoresistance in various human malignancies. SIX1 overexpression in cervical cancer tissues has been linked to increased clinical stage and lymph node metastasis; however, the regulatory function of SIX1 in cervical cancer remains largely unexplored. In this study, we found that SIX1 promotes cervical cancer cell proliferation, invasion, and migration by enhancing glucose metabolism. Additionally, SIX1 was shown to influence the glycolytic process in cervical cancer by upregulating GLUT1, PFK1, PGK1, ENO1, and PKM2 expression. Furthermore, we identified a binding site for SIX1 in the ENO1 promoter region, demonstrating that SIX1 has a regulatory effect. These results suggest that SIX1 regulates proliferation and glucose metabolism in cervical cancer cells by promoting the transcription of key glycolytic enzymes, such as ENO1. Understanding this regulatory mechanism is crucial for identifying potential therapeutic targets for cervical cancer.
The influence of cell source on the senescence of human mesenchymal stem/stromal cells.
Hoseini SM, Montazeri F
Hum Cell · 2025 Apr · PMID 40221541 · Publisher ↗
While mesenchymal stem/stromal cells (MSCs) exhibit the ability to self-renew, they are not immortal; they eventually reach a point of irreversible growth cessation and functional deterioration following a limited series...
While mesenchymal stem/stromal cells (MSCs) exhibit the ability to self-renew, they are not immortal; they eventually reach a point of irreversible growth cessation and functional deterioration following a limited series of population doublings, referred to as replicative senescence. When evaluated according to the criteria set by the International Society for Cell Therapy (ISCT), MSCs show significant differences in their senescence patterns and other characteristics related to their phenotype and function. These differences are attributed to the source of the MSCs and the conditions in which they are grown. MSCs derived from fetal or adult sources have variations in their genome stability, as well as in the expression and epigenetic profile of the cells, which in turn affects their secretome. Understanding the key factors of MSC senescence based on cell source can help to develop effective strategies for regulating senescence and improving the therapeutic potential.
RFX5 promotes the progression of triple-negative breast cancer through transcriptional activation of JAG1.
Li C, Wang X, Shi D … +3 more , Yang M, Yang W, Chen L
Hum Cell · 2025 Apr · PMID 40220043 · Publisher ↗
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by high recurrence rates, low survival rates, and a lack of therapeutic targets. Regulatory Factor X5 (RFX5) is a critical transcr...
Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by high recurrence rates, low survival rates, and a lack of therapeutic targets. Regulatory Factor X5 (RFX5) is a critical transcription factor during tumor progression. However, the role of RFX5 involving breast cancer or TNBC has not been studied. This study obtained 60 tumor samples of TNBC for analysis and ascertained that RFX5 is linked with the severe stage. We constructed RFX5 knockdown and overexpression models involving TNBC cells. RFX5 overexpression enhanced TNBC cell proliferation by detecting cell vitality and replication of DNA and analyzing cell cycle data. RFX5 facilitated cell migration and invasion, which were determined by wound healing and Transwell assays. The anti-apoptotic RFX5 properties were confirmed with Hoechst staining and Annexin V/PI apoptosis assays. The Notch pathway was activated in TNBC, and Jagged canonical Notch ligand 1 (JAG1) could enhance TNBC growth and metastasis. RFX5 upregulation elevated JAG1 mRNA and protein levels. Chromatin immunoprecipitation and luciferase reporter assays indicated that RFX5 promoted the transcriptional activation of JAG1 by binding the promoter (- 1890/+ 15 or - 1359/+ 15 area). JAG1 knockdown reduced RFX5-induced expression of Notch signaling-related factors Notch1, NICD, and Hes1. This paper indicated that RFX5 is a transcription factor for JAG1 and established that RFX5 could activate the Notch pathway via transcriptional activation of JAG1 and promote TNBC progression. Targeting RFX5 could be a promising therapeutic approach against TNBC.
Ovarian Leydig cells and neural crests.
Carrasco-Juan JL, Tapia O, González-Gómez M … +5 more , Vega-Falcón A, García-Hernández S, Rufino-Gómez A, Méndez-Medina R, Álvarez-Arguelles Cabrera H
Hum Cell · 2025 Apr · PMID 40220034 · Full text
In our search for markers to identify and study ovarian Leydig cells, we utilized immunohistochemical techniques and visualized the results using conventional and confocal microscopy. We successfully employed steroidogen...
In our search for markers to identify and study ovarian Leydig cells, we utilized immunohistochemical techniques and visualized the results using conventional and confocal microscopy. We successfully employed steroidogenic factor- 1 (SF1), androgen receptor (AR), and class III β-tubulin as markers. SF1 and AR specifically highlighted the intraneural cell precursors of Leydig cells, which were previously identified in a published case of mature cystic teratoma of the ovary, and the adult ovarian Leydig cells. Furthermore, the transient expression of class III β-tubulin could be associated with the intraneural displacement of these precursors, cooperating in their migration to colonize the ovaries of adult women.
In vitro properties of four benign meningioma cells derived from WHO grade 1 meningiomas.
Trasaktaweesakul T, Asavaritikrai P, Talabnin K … +5 more , Kongnawakul D, Tastub S, Jaturutthaweechot P, Naewwan N, Talabnin C
Hum Cell · 2025 Apr · PMID 40214859 · Publisher ↗
Meningiomas are common intracranial tumors arising from the meninges. They exhibit heterogeneity in their biological behaviors and clinical outcomes. Understanding the molecular mechanisms of meningioma development and p...
Meningiomas are common intracranial tumors arising from the meninges. They exhibit heterogeneity in their biological behaviors and clinical outcomes. Understanding the molecular mechanisms of meningioma development and progression using in vitro systems is essential for improved diagnosis and targeted therapeutic strategies. In this study, four primary meningioma cells designated as SUT-MG9, SUT-MG12, SUT-MG14, and SUT-MG16 were established from WHO grade 1 meningioma tissues via a primary cell culture technique. The phenotypic and genetic characteristics of the four primary meningioma cells were determined. Four primary meningioma cells presented a spindle-shaped morphology with large nuclei and showed prominent expression of meningioma markers, including somatostatin receptor 2 A and vimentin. Growth characteristics demonstrated that SUT-MG9, SUT-MG12, and SUT-MG14 were fast growing, whereas SUT-MG16 was slow growing. Additionally, the expression levels of relevant genes in cell stemness (SOX2, Nanog, and BMI1) and cell cycle (CDK4, CCND1, and CCNB1) were detected only in SUT-MG12 and SUT-MG14. Interestingly, chemosensitivity assay showed that primary benign meningioma cells were less sensitive to gemcitabine and 5-fluorouracil. Moreover, biochemical profiles revealed high lipid and ester contents, but low nucleic acid contents in all primary meningioma cells compared to malignant meningioma cell lines. In conclusion, the four primary meningioma cells can serve as cell models for further meningioma development and drug treatment studies.
LINC01559: roles, mechanisms, and clinical implications in human cancers.
Zhang S, Lan X, Lei L
Hum Cell · 2025 Apr · PMID 40205068 · Publisher ↗
Long intergenic non-protein coding RNA 1559 (LINC01559), a long non-coding RNA (lncRNA) located on chromosome 12p13.1, plays a critical role in the progression of various cancers. The aberrant expression of LINC01559 sig...
Long intergenic non-protein coding RNA 1559 (LINC01559), a long non-coding RNA (lncRNA) located on chromosome 12p13.1, plays a critical role in the progression of various cancers. The aberrant expression of LINC01559 significantly impacts multiple biological processes in tumor cells, including cell proliferation, epithelial-mesenchymal transition (EMT), migration, invasion, angiogenesis, and cellular stemness. Notably, the expression levels of LINC01559 correlate with the pathological features and prognosis of several cancers, such as pancreatic, breast, and gastric cancers, and it may serve as a diagnostic marker for non-small cell lung cancer. Moreover, the expression of LINC01559 is regulated by various mechanisms and can influence cancer initiation and progression through a competing endogenous RNA (ceRNA) network, where it interacts with a cohort of eight different microRNAs (miRNAs). Additionally, LINC01559 may directly interact with downstream proteins, thereby promoting their functions or enhancing their stability. LINC01559 is also implicated in key signaling pathways associated with cancer development, including the PI3 K/AKT, RAS, and autophagy signaling pathways. Furthermore, it has been linked to drug resistance in breast cancer and hepatocellular carcinoma. This review provides a comprehensive assessment of the clinical implications of dysregulated LINC01559 expression across various cancer types, highlighting its crucial functions and underlying molecular mechanisms in tumorigenesis. Additionally, we present in-depth discussions and propose hypotheses regarding the functional roles of LINC01559 in cancer pathogenesis, while outlining potential research avenues for future exploration of this molecular target.
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