Hereditas最新文献

{"title":"RBM15 promotes COAD progression by regulating the m6A modification of TMC5.","authors":"Errong Tian, Li Gao, Lan Wu, Limin Qin","doi":"10.1186/s41065-025-00530-4","DOIUrl":"https://doi.org/10.1186/s41065-025-00530-4","url":null,"abstract":"<p><strong>Background: </strong>Colon adenocarcinoma (COAD) is a frequent digestive system malignancy with high mortality and poor prognosis. Transmembrane Channel-like 5 (TMC5) has been reported to play an oncological role in various cancers. However, the role and mechanism of TMC5 in COAD remain unclear.</p><p><strong>Methods: </strong>TIMER and UALCAN databases analyzed the expression of TMC5 in COAD. TMC5, RNA-binding motif protein-15 (RBM15), E-cadherin, N-cadherin, Vimentin, Fibronectin, and RAD51 protein levels were determined using western blot. TMC5, RBM15, Ferritin heavy chain 1 (FTH1), and cystine/glutamate antiporter SLC7A11 (also commonly known as xCT) mRNA levels were examined using real-time quantitative polymerase chain reaction (RT-qPCR). Cell proliferation, apoptosis, migration, and invasion were assessed using 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, and transwell assays. Caspase 3 activity, ROS level, Fe⁺ level, and glycolysis level were detected using commercial kits. Immunofluorescence assay analyzed 53BP1 and γH2AX foci. Role of TMC5 on COAD tumor growth was examined using xenograft tumor model in vivo. After SRAMP database analysis, interaction between RBM15 and TMC5 was verified using methylated RNA immunoprecipitation (MeRIP) and dual-luciferase reporter assay.</p><p><strong>Results: </strong>TMC5 and RBM15 levels were significantly increased in COAD tissues and cells. Moreover, TMC5 silencing could inhibit COAD cell proliferation, migration, invasion, EMT, glycolysis, and induce apoptosis and ferroptosis in vitro, as well as repress tumor growth in vivo. At the molecular level, RBM15 could sustain RNA stability and TMC5 expression through regulating the m6Amodification.</p><p><strong>Conclusion: </strong>RBM15 could facilitate COAD cell malignant behaviors at least by regulating the stability of TMC5 mRNA, providing a powerful and hopeful target for COAD treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"177"},"PeriodicalIF":2.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395726/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951415","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":"Qingxie Fuzheng granules attenuate cancer cachexia by restoring gut microbiota homeostasis and suppressing IL-6/NF-κB signaling in colorectal adenocarcinoma.","authors":"Yishun Jin, Lisha Lu, Hangju Hua, Biyin Chen, Wenzheng Fang, Kaimin Lin, Peng Ren, Zhenbo Geng, Ling Wang, Xiaohua Yan, Wujin Chen, Jiumao Lin","doi":"10.1186/s41065-025-00541-1","DOIUrl":"https://doi.org/10.1186/s41065-025-00541-1","url":null,"abstract":"<p><p>Cancer cachexia, a debilitating syndrome characterized by muscle wasting and systemic inflammation, remains a major unmet clinical need. Qingxie Fuzheng Granules (QFG), a traditional Chinese medicine formulation, have shown promise in cancer therapy, but their role in cachexia management is unclear.Here, we investigated the anti-cachectic effects of QFG in a murine model of colon adenocarcinoma-induced cachexia. 16S rRNA sequencing revealed gut dysbiosis in cachectic mice, with increased Enterobacteriaceae and decreased Lactobacillus. QFG treatment restored microbial balance, reduced pro-inflammatory cytokines TNF-α, IL-6, and enhanced intestinal barrier integrity by upregulating tight junction proteins ZO-1, Occludin, Calprotectin.Mechanistically, QFG rebalanced Th17/Treg cell ratios and suppressed IL-6/NF-κB signaling, a key driver of muscle atrophy. Combining QFG with glutamine (Gln) further amplified these effects, suggesting synergistic therapeutic potential.Our findings demonstrate that QFG ameliorates cancer cachexia through microbiota modulation and IL-6/NF-κB inhibition, providing a novel multi-targeted approach for cachexia treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"178"},"PeriodicalIF":2.5,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12398093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951460","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":"Decoding the PTTG family's contribution to LUAD pathogenesis: a comprehensive study on expression, epigenetics, and therapeutic interventions.","authors":"Jinna Di, Li Tian, Fan Yan, Zhang Zhe, Cai Lin, Liu Jingyu","doi":"10.1186/s41065-025-00545-x","DOIUrl":"https://doi.org/10.1186/s41065-025-00545-x","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) stands as a prevalent malignancy, yet its pathology remains incompletely comprehended.</p><p><strong>Methods: </strong>In this comprehensive study, we explored the roles of the pituitary tumor-transforming gene (PTTG) family, including PTTG1, PTTG2, and the pseudogene PTTG3P in lung adenocarcinoma (LUAD). Employing a multi-faceted approach, we conducted in-depth analyses using clinical samples and expression datasets.</p><p><strong>Results: </strong>Our findings revealed a significant up-regulation of PTTG family genes in LUAD cell lines and tissue samples compared to adjacent normal controls, suggesting their potential as diagnostic biomarkers. Through promoter methylation and mutational analyses, we uncovered regulatory mechanisms influencing PTTG gene expression. The exploration of the PTTG family's impact on LUAD patient survival demonstrated their association with adverse outcomes, emphasizing their potential prognostic relevance. Moreover, functional assays demonstrated that the knockdown of PTTG1 and PTTG2 genes resulted in the reduction of cell proliferation, colony formation, and cell migration abilities in A549 and H1975 LUAD cells. Furthermore, our investigation extended to therapeutic avenues, where we identified Calcitriol as a potential drug within the DrugBank database to down-regulate PTTG genes. Molecular docking analyses provided insights into the strong interaction between Calcitriol and PTTG1/PTTG2 proteins, laying the groundwork for further exploration of Calcitriol in LUAD treatment.</p><p><strong>Conclusion: </strong>In conclusion, this study contributes a comprehensive understanding of the PTTG family's involvement in LUAD, shedding light on their diagnostic, prognostic, and therapeutic implications.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"175"},"PeriodicalIF":2.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12395852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144951748","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":"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":"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":"Identification of anoikis-related genes in heart failure: bioinformatics and experimental validation.","authors":"Lina Zhang, Jianjun Gu, Yan Jiang, Juan Xue, Ye Zhu","doi":"10.1186/s41065-025-00532-2","DOIUrl":"10.1186/s41065-025-00532-2","url":null,"abstract":"<p><strong>Background: </strong>Heart failure (HF) is a common clinical syndrome caused by ventricular dysfunction and one of the leading causes of mortality worldwide. Previous studies have suggested that anoikis is relevant to HF. This study aimed to identify hub genes associated with anoikis that may offer therapeutic targets for HF.</p><p><strong>Materials and methods: </strong>Gene expression data for GSE36074 were obtained from the Gene Expression Omnibus (GEO) and anoikis-related genes (ARGs) were extracted from GeneCards. GEO2R was used to screen for differentially expressed genes (DEGs), then by overlapping DEGs with ARGs, differentially expressed ARGs (DEARGs) were screened. The biological functions of the DEARGs were determined using DAVID. Subsequently, two machine learning (ML) algorithms were employed to identify hub DEARGs: least absolute shrinkage and selection operator (LASSO) and random forest (RF). In addition, miRNA-hub DEARGs and drug-hub DEARGs networks were constructed. Lastly, the hub DEARGs were validated by quantitative reverse transcription PCR (RT-qPCR) and Immunofluorescence (IF).</p><p><strong>Results: </strong>A total of 138 DEARGs were identified in GSE36074. Functional analysis of DEARGs revealed that they were primarily enriched in the positive regulation of the apoptotic process, PI3K-Akt, and FoxO signaling pathways. Subsequently, two hub DEARGs (Tln1 and TGFβ2) were screened using LASSO and RF algorithms. According to the miRNA-hub DEARGs networks, Tln1 and TGFβ2 were regulated by 34 and 68 miRNAs, respectively. Moreover, drug-hub DEARGs networks showed that Gemogenovatucel-t, Lerdelimumab, Belagenpumatucel-l, Fresolimumab, Bintrafusp alfa, Trabedersen and Luspatercept-aamt are potential drugs that could target TGFβ2. Finally, RT-qPCR and IF validation of two key DEARGs (Tln1 and TGFβ2) supported our bioinformatics analysis.</p><p><strong>Conclusions: </strong>These findings suggest that Tln1 and TGFβ2 may play important roles in HF development through the regulation of anoikis and may serve as therapeutic targets for HF.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"163"},"PeriodicalIF":2.5,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357471/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862189","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":"Programmed death 1 inhibitor combined with radiotherapy decreases epidermal growth factor receptor expression in breast cancer.","authors":"You Wu","doi":"10.1186/s41065-025-00472-x","DOIUrl":"10.1186/s41065-025-00472-x","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of programmed death 1 (PD-1) inhibitors combined with radiotherapy on the expression of P53 and epidermal growth factor receptor (EGFR) in breast cancer (BC). The impact of radiation treatment on BC patients' prognosis was examined.</p><p><strong>Methods: </strong>The data of BC patients admitted to Nanjing University of Chinese Medicine from April 2022 to April 2023 were retrospectively analyzed. The clinical data of the patients were extracted, and 104 patients were randomly enrolled. The survival time and complications of patients were followed up. The expression levels of P53 and EGFR in tumor tissues and prognosis of patients treated with PD-1 inhibitor combined with radiotherapy were analyzed.</p><p><strong>Result: </strong>The expression level of EGFR in the joint group (JG) was visibly lower as against the control group (CG); The median progression-free survival (PFS) of the JG was visibly longer as against the CG (all P < 0.05). The optimal cut-off values of P53 positive rate and EGFR level before combined treatment were 10% and 96.21ng/mL. In addition, the median PFS of individuals with low EGFR in the JG was 7.3, which was visibly higher as against individuals with high EGFR. The level of EGFR before PD-1 inhibitor treatment was an independent cause of risk affecting the prognosis of patients.</p><p><strong>Conclusion: </strong>PD-1 inhibitor plus radiotherapy can effectively inhibit the expression of EGFR in tumor tissues of BC patients and visibly improve the prognosis.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"160"},"PeriodicalIF":2.5,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862191","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 approach reveals CCND1, GABPA, HIF1A, and SOX6 as key regulators and prognostic markers in heart failure.","authors":"Ping He, Lang Deng, Kaijie Wu","doi":"10.1186/s41065-025-00536-y","DOIUrl":"10.1186/s41065-025-00536-y","url":null,"abstract":"<p><strong>Introduction: </strong>Heart failure (HF) is a progressive condition with complex molecular mechanisms. This study aims to identify potential biomarkers and therapeutic targets by analyzing differentially expressed genes (DEGs) in HF patients, exploring the roles of hub genes, and developing a risk model for predicting disease progression.</p><p><strong>Methodology: </strong>We cultured five human HF cell lines and five normal coronary cardiomyocyte cell lines. Gene expression datasets were retrieved from the Gene Expression Omnibus (GEO) database and analyzed using limma. Protein-Protein Interaction (PPI) networks were constructed with STRING, and immune cell infiltration was analyzed using CIBERSORT. A risk model was built using LASSO regression. Drug screening was performed via CMap, and overexpression studies of CCND1 and HIF1A were conducted in AC16 and SEKHEP1 cells via cell proliferation, colony formation, and wound healing assays.</p><p><strong>Results: </strong>We identified 182 common DEGs associated with HF. Hub genes CCND1, GABPA, HIF1A, and SOX6 were central in the PPI network. LASSO regression established a risk model linked to disease progression. Immune infiltration analysis revealed altered immune cell profiles in HF. The miRNA-mRNA network showed interactions of hsa-miR-93-5p, hsa-miR-802, hsa-miR-199a-5p, and hsa-miR-203a-3p with hub genes. Overexpression of CCND1 and HIF1A in cell lines impaired proliferation, colony formation, and migration, implicating their role in HF pathophysiology.</p><p><strong>Conclusion: </strong>CCND1, GABPA, HIF1A, and SOX6 may serve as biomarkers for HF. Our findings provide valuable insights into immune infiltration, miRNA regulation, and the identification of therapeutic targets for HF management. These results highlight the role of gene regulation in HF progression and may guide future therapeutic interventions.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"165"},"PeriodicalIF":2.5,"publicationDate":"2025-08-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12357434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144862190","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}