Hereditas最新文献

{"title":"HOXA13 promotes high glucose-induced trophoblast cell growth and migration during gestational diabetes by regulating the smad2 pathway.","authors":"Fei Zhao, Xinhong Liu, Hong Qin","doi":"10.1186/s41065-025-00542-0","DOIUrl":"https://doi.org/10.1186/s41065-025-00542-0","url":null,"abstract":"<p><strong>Background: </strong>Gestational diabetes mellitus (GDM) is considered the most common complication of pregnancy, and is a very dangerous disease for both mother and baby. Homeobox A13 (HOXA13) has been discovered to join into some diseases through exhibiting regulatory functions. Importantly, hypermethylation of HOXA13 has been observed in the placental tissues of preeclampsia. However, the regulatory impacts of HOXA13 on GDM progression keep dimness.</p><p><strong>Methods: </strong>The GDM cell model and GDM rat model were established. The expressions of genes were measured through RT-qPCR, western blot or IHC assay. The cell proliferation was tested through MTT and Edu assays. The cell migration was determined through Transwell assay. The fasting blood glucose of rats was detected through the blood glucose meter.</p><p><strong>Results: </strong>HOXA13 was verified to be lowly expressed in placental tissues from GDM patients. In addition, the cell proliferation and migration abilities of trophoblast cells were attenuated after high glucose (HG) treatment, but these impacts were counteracted after HOXA13 overexpression. It was further demonstrated that HOXA13 affected the proliferation and migration abilities of HG-triggered trophoblast cells by enhancing smad2 expression. At last, it was testified that HOXA13 can ameliorate GDM symptoms in vivo.</p><p><strong>Conclusion: </strong>This study manifested that HOXA13 accelerated HG-triggered trophoblast cell growth and migration by regulating the smad2 pathway. This discovery hinted that HOXA13 may be a target for ameliorating GDM.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"176"},"PeriodicalIF":2.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The methylation site cg06972019 regulates the succinylation-related gene ENO1 to inhibit the occurrence of erectile dysfunction.","authors":"Jian Wang, Siyuan Ye, Maoxiao Xu, Mengru Sun, Yang Lu, Zhenrong Piao, Fengmeng Teng, Maosen Zhang","doi":"10.1186/s41065-025-00543-z","DOIUrl":"https://doi.org/10.1186/s41065-025-00543-z","url":null,"abstract":"<p><strong>Background: </strong>This study aims to explore the causal relationship between the expression of succinylation-related genes and erectile dysfunction (ED).</p><p><strong>Method: </strong>Through a literature review, we identified 19 succinylation-related genes and intersected them with cis-expression Quantitative Trait Loci (cis-eQTL) data from the eQTLGen Consortium, ultimately selecting 16 genes with available cis-eQTL data. Subsequently, we downloaded genomic data related to erectile dysfunction (ED) from 223,805 European male participants in the IEU OpenGWAS project and performed a two-sample Mendelian Randomization (MR) analysis. Summary-based Mendelian Randomization (SMR) analysis and ELISA testing further confirmed the statistical association between ENO1 gene expression and ED risk. Mediation analysis was used to explore the potential regulatory role of DNA methylation in the relationship between gene expression and ED.</p><p><strong>Result: </strong>Through MR analysis, a significant causal relationship between the ENO1 gene and ED was identified. The results indicated that the expression of the ENO1 gene has a significant causal effect on the risk of ED (OR: 1.2388, 95% CI: 1.0708-1.4332, p < 0.05). SMR analysis further confirmed the causal relationship between ENO1 gene expression and ED (SMR_p-value = 0.0040). Mediation analysis suggested that the methylation site cg06972019 may inhibit the occurrence of ED by regulating ENO1, with the mediation proportion accounting for 67.6% of the total effect (P = 0.0013). ELISA results showed that the serum ENO1 levels in ED patients were significantly higher than those in the healthy control group (p < 0.05), validating the potential role of ENO1 in ED.</p><p><strong>Conclusion: </strong>This study revealed the potential causal relationship of the ENO1 gene in the development of ED through Mendelian Randomization and SMR analysis, further validating the association between gene expression and ED. The overexpression of the ENO1 gene may be regulated by the methylation site cg06972019. These findings provide new insights into the molecular mechanisms of ED and may offer new biomarkers for the early diagnosis and targeted treatment of ED.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"172"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research landscape of photodynamic therapy for hepatocellular carcinoma: Hotspots and Prospects from 2012 to 2025.","authors":"Fei Yu, Sihan Yin, Jiayu Zhu, Kewei Sun","doi":"10.1186/s41065-025-00509-1","DOIUrl":"https://doi.org/10.1186/s41065-025-00509-1","url":null,"abstract":"<p><strong>Objective: </strong>To explore the current status and future development of photodynamic therapy (PDT) for hepatocellular carcinoma (HCC). However, this field lacks a comprehensive bibliometric analysis. This study aims to investigate the research content and hotspots in PDT for liver cancer from 2012 to 2025, and to predict future research directions, providing references for subsequent studies.</p><p><strong>Methods: </strong>We chose the Web of Science Core Collection (WoSCC) database and retrieved articles published in the field between 2012 and 2025. Bibliometric and visualization analyses were performed using R (version 4.4.1), VOSviewer (version 1.6.19), and CiteSpace (version 6.4. R1).</p><p><strong>Results: </strong>A total of 547 papers were included. We found that the number of publications in this field has steadily increased from 2012 to 2025. China leads with the highest number of publications, followed by the USA, Korea, Germany, and Japan. China has the lowest international co-authorship rate, while Germany and Japan show higher international collaboration rates. The International Journal of Nanomedicine is the most popular journal for publication, whereas Biomaterials ranks first in terms of citations. Our analysis of keywords and the most cited references revealed that current research focuses on the mechanism of PDT-induced apoptosis in HCC, the development of photosensitizers (PSs), nanotechnology-enhanced PDT, and synergistic treatment of HCC with PDT and other therapies. Nanotechnology and multimodal synergistic therapeutic strategies are driving the treatment of HCC.</p><p><strong>Conclusion: </strong>PDT, as a therapy for HCC, is expected to become a research hotspot. This paper analyzes PDT's current research for HCC, offering references for future research in related fields.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"174"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382027/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The diagnostic and prognostic value of LncRNA FAM3D-AS1 expression in nasopharyngeal carcinoma and its effect on tumor progression and cisplatin resistance.","authors":"Bohan Zhang, Zixiao Chen, Zhinong Wu","doi":"10.1186/s41065-025-00526-0","DOIUrl":"https://doi.org/10.1186/s41065-025-00526-0","url":null,"abstract":"<p><strong>Background: </strong>The location of nasopharyngeal carcinoma (NPC) is relatively hidden. Most patients are diagnosed at the middle or late stage of the disease, having missed the best time for treatment.</p><p><strong>Aim: </strong>To explore the clinical value of lncRNA FAM3D-AS1 and its effect on tumor progression and cisplatin resistance in nasopharyngeal cancer.</p><p><strong>Materials and methods: </strong>In this study, a total of 118 NPC patients and 50 healthy volunteers participated. RT-qPCR was analyzed to detect the lncRNA FAM3D-AS1 expression in NPC patients and cells. Receiver Operating Characteristic (ROC curves), Kaplan-Meier (K-M) survival curves and Cox regression analysis were performed to analyze the clinical value value of lncRNA FAM3D-AS1. Cell functional assays were employed to investigate the impact of lncRNA FAM3D-AS1 on biological malignant behavior of NPC and cisplatin resistance.</p><p><strong>Results: </strong>In NPC patients' serum and cell lines, the expression of lncRNA FAM3D-AS1 was upregulated. ROC curves with Area Under the Curve (AUC) = 0.920, 95%CI = 0.874-0.965 could be used to distinguish the healthy group from the NPC group. K-M survival curves revealed that NPC patients with high expression of lncRNA FAM3D-AS1 had poor prognosis. Cox regression analysis suggested that lncRNA FAM3D-AS1 was an independent prognostic marker for NPC. Knockdown of lncRNA FAM3D-AS1 expression prohibited NPC cell proliferation, migration, invasion, and cisplatin resistance, but promoted apoptosis.</p><p><strong>Conclusion: </strong>LncRNA FAM3D-AS1 can be used as a biomarker to diagnose and prognosticate NPC. LncRNA FAM3D-AS1 affects tumor progression and cisplatin resistance in NPC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"171"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951533","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrated single-cell and bulk transcriptomic profiling reveals cancer-associated fibroblast heterogeneity in glioblastoma and establishes a clinically actionable prognostic model and preliminary experimental validation.","authors":"Wenhua Zhang, Yaxiong Li, Conghui Li, Qiang Huang","doi":"10.1186/s41065-025-00548-8","DOIUrl":"https://doi.org/10.1186/s41065-025-00548-8","url":null,"abstract":"<p><p>Cancer-associated fibroblasts (CAFs) critically regulate tumor progression, angiogenesis, metastasis, and therapeutic resistance. This study investigated the characteristics of CAFs in glioblastoma (GBM) and developed a CAF-based risk signature to predict patient prognosis. The single-cell RNA sequencing (scRNA-seq) data were sourced from the Gene Expression Omnibus (GEO) database, whereas the bulk RNA-seq datasets were retrieved from The Cancer Genome Atlas (TCGA) and Chinese Glioma Genome Atlas (CGGA), respectively. The Seurat R package processed scRNA-seq data to identify CAF clusters using established markers. Prognostic genes were screened through univariate Cox regression, with Lasso regression constructing the final risk model. A nomogram incorporating clinical parameters was subsequently developed. Immunohistochemical validation was performed using the Human Protein Atlas (HPA) for the signature genes. The qRT-PCR validation was conducted in U251 and HA cells. ScRNA-seq analysis revealed five CAF clusters in GBM, including three prognostically relevant subtypes. Three key genes were refined to construct a risk signature functionally enriched in the the IL6_JAK_STAT3 signaling, P53 pathway, and inflammatory response. The signature correlated strongly with stromal and immune scores. Multivariate analysis confirmed risk signature independent prognostic value (P < 0.0001), followed by age (P = 0.005). The CAF-derived nomogram demonstrated superior predictive accuracy for 1-/2-year survival compared to clinical factors alone. The signature genes were validated in the HPA database and experimental validation. This study proposes CAF-derived molecular signatures as potential predictors of glioblastoma prognosis worthy of clinical validation. Systematic characterization of CAF heterogeneity may offer insights for interpreting GBM immunotherapy responses, providing a foundation for future exploration of stroma-targeted therapeutic strategies.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"173"},"PeriodicalIF":2.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12382188/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951410","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Damnacanthus giganteus extract block diffuse large b-cell lymphoma proliferation and EMT by regulating mitochondrial dysfunction and glycolysis.","authors":"Peng Yang, GuangYun Zhou, XiuMei Ma, MingTao Huang, ZuJie Qin, Bing Qing, SuLing Chen, JiangCun Wei","doi":"10.1186/s41065-025-00531-3","DOIUrl":"https://doi.org/10.1186/s41065-025-00531-3","url":null,"abstract":"<p><strong>Background: </strong>In non-Hodgkin's lymphoma, diffuse large b-cell lymphoma (DLBCL) is one of the most prevalent and commonly diagnosed subtypes. There is a need to develop more effective drugs since the currently approved drugs still have limitations.</p><p><strong>Methods: </strong>DLBCL cell lines were intervened with different concentrations of Damnacanthus giganteus extract (DGE). The malignant phenotype of DLBCL cells was detected by CCK-8, colony formation assay, AnnexinV-PI double staining assay, and Transwell. The effect of DGE on the in vivo growth of DLBCL cells was assessed by nude mice transplantation tumor assay and immunohistochemistry. Cellular mitochondrial function was assessed by measuring mitochondrial ROS levels, MMP, and ATP production, and glycolysis was assessed by determining glucose uptake and lactate production. The changes of epithelial-mesenchymal transition (EMT) markers were evaluated via Western blot.</p><p><strong>Results: </strong>Intervention with low-toxicity concentrations of DGE significantly inhibited proliferative capacity and clonogenic potential in DLBCL cells while concurrently enhancing apoptosis and cisplatin sensitivity. DGE treatment also suppressed migratory and invasive behaviors, accompanied by downregulation of mesenchymal markers N-cadherin and Vimentin. In vivo studies confirmed therapeutic efficacy, with DGE monotherapy showing marked tumor growth suppression and synergistic activity with cisplatin. Mechanistically, DGE exacerbated mitochondrial dysfunction and suppressed glycolysis. This mitochondrial impairment phenotype elicited by DGE treatment was recapitulated using the mitochondrial complex I inhibitor Rotenone, which similarly induced proliferation inhibition and EMT modulation. Furthermore, the ROS scavenger N-acetylcysteine partially rescued DGE-induced cellular alterations, including proliferation and EMT suppression.</p><p><strong>Conclusion: </strong>‌Our study demonstrates for the first time that DGE effectively suppresses tumor proliferation and EMT during DLBCL progression. These antitumor effects appear to be mediated through modulation of mitochondrial function and glycolysis. These findings position DGE as a promising novel therapeutic candidate for DLBCL treatment, meriting immediate clinical translation and further evaluation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"170"},"PeriodicalIF":2.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12379491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951767","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-associated genes and metabolic abnormalities in peripheral blood mononuclear cells of type 1 diabetes mellitus patients.","authors":"Wen-Biao Ma, Xue-Ying Wang, Yuan-Yuan Zuo","doi":"10.1186/s41065-025-00537-x","DOIUrl":"https://doi.org/10.1186/s41065-025-00537-x","url":null,"abstract":"<p><strong>Background: </strong>Type 1 diabetes mellitus (T1DM) is a chronic autoimmune disorder characterized by insulin deficiency, which causes hyperglycemia and systemic metabolic dysregulation.</p><p><strong>Methods: </strong>In this study, we used the gene expression dataset GSE156035 to identify differentially expressed genes (DEGs) between healthy controls and patients with T1DM. Functional enrichment analysis, Gene Ontology analysis, and protein-protein interaction network analysis were employed to identify hub genes.</p><p><strong>Results: </strong>We observed significant upregulation and downregulation of DEGs. Upregulated genes were primarily involved in TGF-beta signaling and retinol metabolism, while downregulated genes were associated with MAPK signaling and circadian rhythm pathways. Crucial cellular processes, such as neutrophil activation, defense response to fungi, and neuron differentiation, were highlighted. Hub genes, such as FOS, JUNB, NR4A2, and DUSP1, were identified and showed strong correlations with key signaling pathways. Additionally, elevated levels of angiogenesis, epithelial-mesenchymal transition, and hypoxia in T1DM were indicated, along with significant alterations in metabolite levels, including glucose, leucine, and phenylalanine, and their correlations with hub genes.</p><p><strong>Conclusion: </strong>These findings not only identify specific hub genes as key mediators connecting signaling pathways, biological processes, and metabolic changes but also provide novel insights into the pathophysiology of T1DM.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"168"},"PeriodicalIF":2.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369233/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of circ_0091761 ameliorates acute myocardial infarction-induced endothelial injury through regulation of miR-1278.","authors":"Bin Zhou, Haitao Wang, Kun Zhang, Jin Xie, Cuicui Yuan, Jia Jin, Jian Zhang, Meng Ma, Zhengnan Zhang","doi":"10.1186/s41065-025-00519-z","DOIUrl":"https://doi.org/10.1186/s41065-025-00519-z","url":null,"abstract":"<p><strong>Objective: </strong>The main objective of the article was to explore the role of circ_0091761 in acute myocardial infarction (AMI)-induced endothelial injury.</p><p><strong>Methods: </strong>A cellular model of AMI was constructed by hypoxia-induced HUVECs. miRNAs that may interact with circ_0091761 were recognized by the ENCORI and circular RNA Interactom databases. RT-qPCR was performed to analyze the levels of circ_0091761 in AMI patients as well as miR-1278, ICAM1, and VCAM1 in hypoxia-induced HUVECs. Flow cytometry was used to detect apoptosis. ROS kit and LDH kit were used to detect the levels of ROS and LDH, respectively. Dual-luciferase reporter assay, RIP assay, and RNA pull-down assay were performed to validate their interaction between circ_0091761 and miR-1278.</p><p><strong>Results: </strong>circ_0091761 was elevated in AMI patients compared to healthy controls. Silencing circ_0091761 reduced apoptosis, ICAM1, and VCAM1 levels, as well as ROS and LDH. circ_0091761 could interact with miR-1278 and negatively regulate miR-1278 expression in hypoxia-induced HUVECs. At the same time, inhibiting miR-1278 reverses the protective effect of transfected si-circ_0091761 on HUVECs.</p><p><strong>Conclusion: </strong>Down-regulation of circ_0091761 ameliorates AMI-induced endothelial injury by targeting miR-1278.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"169"},"PeriodicalIF":2.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12369235/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM15 enhances paclitaxel resistance in triple-negative breast cancer by targeting m⁶A methylation of TNFSF9 and inducing polarization of tumor-associated macrophages to M2 phenotype.","authors":"Jinkun Fu, Chao Wei, Yijian Chen, Xiaoming He, Kun Zhang","doi":"10.1186/s41065-025-00534-0","DOIUrl":"10.1186/s41065-025-00534-0","url":null,"abstract":"<p><strong>Background: </strong>Triple-negative breast cancer (TNBC) is one of the breast cancer subtypes with a poor prognosis, and the current main treatment modalities include surgical resection and adjuvant chemotherapy. However, the development of drug resistance in tumor cells to chemotherapeutic agents poses great challenges to anticancer treatment.</p><p><strong>Methods: </strong>Bioinformatics analysis was used to screen the up-regulated genes in paclitaxel (PTX)-resistant TNBC cells. Cell viability was measured by a CCK-8 kit. TNFSF9 (Tumor necrosis factor receptor superfamily member 9) protein level was detected by Western blot (WB) assay. PTX-resistant TNBC cell lines (MDA-MB-231/PTX, MDA-MB-468/PTX) were constructed and their drug resistance was shown by IC50. The EdU, flow cytometry, Transwell, and other commercial kits were applied to detect the proliferation, apoptosis, migration, invasion, macrophage M2 polarization, and glycolysis of PTX-resistant TNBC cells. RBM15 (RNA binding motif protein 15) levels were measured by RT-qPCR and WB assays. The RIP, MeRIP, and actinomycin D assays were used to analyze the interaction between TNFSF9 and RBM15. The effect of RBM15/TNFSF9 on PTX sensitivity in vivo was verified by xenograft tumor experiments.</p><p><strong>Results: </strong>TNFSF9 was highly expressed in PTX-resistant TNBC cells. Silencing of TNFSF9 enhanced the sensitivity to PTX. Silencing TNFSF9 induced polarization of macrophages from M2 to M1 phenotype and the release of IL-1β and TNF-α, but decreased the levels of IL-10 and TGF-β. RBM15 targeted the N6-adenylate methylation (m⁶A) modification of TNFSF9, and overexpression of TNFSF9 could reverse the tumor-suppressing effect of silencing RBM15 on PTX-resistant TNBC cells in vitro and transplanted tumors in vivo. Samples from PTX-sensitive and PTX-resistant TNBC patients proved that RBM15 regulated TNFSF9's high expression in PTX-resistant TNBC tissues.</p><p><strong>Conclusion: </strong>This study demonstrated that RBM15 enhanced PTX resistance in TNBC by promoting m⁶A methylation in TNFSF9 and inducing M2 polarization of tumor-associated macrophages.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"167"},"PeriodicalIF":2.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12362948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882784","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Multi-Omics analysis and in vitro validation reveal diagnostic and therapeutic roles of novel hub genes in ovarian cancer.","authors":"Jianmin Wang, Guanghui Song, Lili Xing","doi":"10.1186/s41065-025-00535-z","DOIUrl":"10.1186/s41065-025-00535-z","url":null,"abstract":"<p><p>Ovarian cancer (OC) remains a highly lethal gynecologic malignancy due to late diagnosis and limited therapeutic options. In this study, we aimed to identify and functionally validate novel hub genes associated with OC progression. We integrated four GEO microarray datasets (GSE54388, GSE40595, GSE18521, and GSE12470) to identify differentially expressed genes (DEGs) between OC and healthy tissues using the limma package. A total of 22 common DEGs were identified, of which four-SNRPA1, LSM4, TMED10, and PROM2-emerged as hub genes based on PPI network centrality. Expression analyses using TCGA data and RT-qPCR confirmed the significant upregulation of these genes in OC samples. Promoter methylation analysis showed hypomethylation in tumors, while ROC analysis revealed high diagnostic accuracy (AUC = 1.0). Although these genes were not significantly associated with overall survival in meta-analysis, they were strongly involved in oncogenic pathways such as EMT, apoptosis, and DNA repair. Predicted miRNAs (e.g., hsa-miR-1178-5p and hsa-miR-31-5p) targeting hub genes were significantly downregulated in OC cell lines. Immune analysis indicated that hub gene expression was correlated with immune subtypes, checkpoint inhibitors, and reduced immune infiltration. Drug sensitivity analysis suggested that high expression of TMED10 and PROM2 may confer susceptibility to chemotherapeutic agents. Functional assays following siRNA-mediated knockdown of TMED10 and PROM2 in A2780 and OVCAR3 cells revealed significant reductions in proliferation, colony formation, and migration. These findings highlight SNRPA1, LSM4, TMED10, and PROM2 as potential diagnostic markers and therapeutic targets in OC, warranting further investigation for clinical translation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"166"},"PeriodicalIF":2.5,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12363112/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144872826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}