{"title":"Identification of mitophagy-related genes in patients with acute myocardial infarction.","authors":"Ju-Ying Li, Hong-Kui Chen, Yi-Hao Huang, Yu-Peng Zhi, Yue-E Li, Kai-Yang Lin, Chun Chen, Yan-Song Guo","doi":"10.1186/s41065-025-00424-5","DOIUrl":"https://doi.org/10.1186/s41065-025-00424-5","url":null,"abstract":"<p><p>Mitophagy is involved in acute myocardial infarction (AMI) process. However, the role of mitophagy-related genes (MRGs) in the AMI process is not well illustrated. We identified MRGs involved in AMI by bioinformatics analysis. The external datasets were employed for the validation of the MRGs, alongside the execution of cellular and animal experiments. Forty-five MRGs were detected, and machine learning identified the top four hub genes, namely ALDH2, ACSL1, IL1B, and GABARAPL1. Additionally, an external validation set was used to screen for three diagnostic markers (ACSL1, IL1B, and GABARAPL1) among these hub genes. Immune infiltration analysis revealed changes in the immune microenvironment among patients with AMI. Finally, the significant upregulation of ACSL1, IL1B, and GABARAPL1 in both cellular and animal models was confirmed. The occurrence of mitophagy was observed in the cell model through transmission electron microscopy (TEM). Our study demonstrated that ACSL1, IL1B, and GABARAPL1 possess potential biomarkers for AMI.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"70"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034215/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994332","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}
HereditasPub Date : 2025-04-25DOI: 10.1186/s41065-025-00433-4
Junaid Abid, Mahmood Basil A Al-Rawi, Ahmad Mahmood, An Li, Tiemin Jiang
{"title":"Correction: Identification and functional characterization of key biomarkers in diffuse large B-cell lymphoma: emphasis on STYX as a prognostic marker and therapeutic target.","authors":"Junaid Abid, Mahmood Basil A Al-Rawi, Ahmad Mahmood, An Li, Tiemin Jiang","doi":"10.1186/s41065-025-00433-4","DOIUrl":"10.1186/s41065-025-00433-4","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"69"},"PeriodicalIF":2.7,"publicationDate":"2025-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12032749/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143962273","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}
HereditasPub Date : 2025-04-22DOI: 10.1186/s41065-025-00435-2
Mustafa Vakur Bor
{"title":"Novel variants require established frameworks: emphasizing the role of ISTH diagnostic and classification guidelines in congenital fibrinogen disorders.","authors":"Mustafa Vakur Bor","doi":"10.1186/s41065-025-00435-2","DOIUrl":"https://doi.org/10.1186/s41065-025-00435-2","url":null,"abstract":"<p><p>This commentary aims to highlight the importance of applying the diagnostic and classification guidelines of the International Society on Thrombosis and Haemostasis (ISTH), along with standardized bleeding assessment tools, in the evaluation of patients with congenital fibrinogen disorders. Additionally, it addresses key laboratory methodologies relevant to the diagnosis of these conditions. We believe that this commentary will contribute meaningfully to the ongoing discussions and promote the adoption of standardized approaches in the assessment of rare congenital fibrinogen disorders.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"68"},"PeriodicalIF":2.7,"publicationDate":"2025-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12013131/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983226","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}
HereditasPub Date : 2025-04-21DOI: 10.1186/s41065-025-00434-3
Xu Huang, Zhihong Pan, Lei Shen, Huan Chen, Chang Chen, Tingting Lv, Yuzhou Mei
{"title":"The mechanism of Weiqi decoction treating gastric cancer: a work based on network pharmacology and experimental verification.","authors":"Xu Huang, Zhihong Pan, Lei Shen, Huan Chen, Chang Chen, Tingting Lv, Yuzhou Mei","doi":"10.1186/s41065-025-00434-3","DOIUrl":"https://doi.org/10.1186/s41065-025-00434-3","url":null,"abstract":"<p><strong>Background: </strong>Weiqi Decoction (WQD) is an empirical prescription traditionally used in China for the treatment of precancerous gastric cancer (GC) lesions. This study aimed to elucidate the potential pharmacological mechanisms of WQD in GC therapy.</p><p><strong>Methods: </strong>Active ingredients, corresponding targets, and GC-related genes were identified using public databases. A protein-protein interaction (PPI) network was constructed via the STRING database, and functional enrichment analyses were conducted using the DAVID platform. Gene expression and survival analyses were performed using the GEPIA database. Molecular docking was conducted with AutoDock Vina and visualized using PyMOL. The effects of WQD on GC cell viability, proliferation, migration, and invasion were evaluated through CCK-8, colony formation, and Transwell assays.</p><p><strong>Results: </strong>WQD contained 43 active ingredients targeting 751 potential genes, including 458 GC-related targets. Quercetin, luteolin, and kaempferol were identified as key active compounds. PPI network analysis revealed nine core targets, including TP53 and SRC, which may mediate the anti-GC effects of WQD. GO enrichment analysis indicated involvement in 726 biological processes, 91 cellular components, and 177 molecular functions, while KEGG pathway analysis suggested modulation of the AGE-RAGE, PI3K-Akt, and HIF-1 signaling pathways. GEPIA database analysis confirmed that EP300, HSP90AA1, HSP90AB1, SRC, and TP53 were highly expressed in GC. Molecular docking demonstrated strong binding affinities between the key active compounds and core targets. In vitro experiments further validated that WQD extract inhibited GC cell viability, proliferation, migration, and invasion.</p><p><strong>Conclusion: </strong>WQD exhibits therapeutic potential against GC by regulating multiple targets and signaling pathways. These findings provide mechanistic insights into the pharmacological actions of WQD in GC treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"67"},"PeriodicalIF":2.7,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012975/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063622","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}
HereditasPub Date : 2025-04-21DOI: 10.1186/s41065-025-00432-5
Bai-Yang Lin, Li Bai, Sheng-Long Wang
{"title":"Regulation of the Nrf2/HO-1 pathway in chronic obstructive pulmonary disease-induced muscle atrophy using Jinshui Liujian decoction and Bajitian pills: insights from network pharmacology and animal models.","authors":"Bai-Yang Lin, Li Bai, Sheng-Long Wang","doi":"10.1186/s41065-025-00432-5","DOIUrl":"https://doi.org/10.1186/s41065-025-00432-5","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to investigate the therapeutic effects of the combination of modified Jinshui Liujian decoction and Bajitian pills (TCM) on chronic obstructive pulmonary disease (COPD)-induced muscle atrophy using network pharmacology and animal model experiments.</p><p><strong>Methods: </strong>Network pharmacology technique has been employed to analyze the potential targets of TCM on treating COPD. In vivo, COPD mice model was induced by lipopolysaccharide (LPS) combined with smoke treatment. To comparing the protective effects of TCM on this disease, these parameters including general condition, serum inflammatory factors, protein expression levels, gene copies, and histopathological changes in the lungs and gastrocnemius muscle mass have been further assessed in mouse in different groups.</p><p><strong>Results: </strong>Network pharmacology analysis identified 203 intersecting targets, primarily associated with apoptosis, phosphorylation, and inflammatory response. Animal experimental demonstrated that TCM could significantly improve the decreased skeletal muscle mass (p < 0.001), abnormal histopathologic morphology, decreased superoxide dismutase (SOD, p < 0.05), increased levels of serum malondialdehyde (MDA, p < 0.001) and tumor necrosis factor-α (TNF-α, p < 0.001) as compared to model group. Further mechanism exploration showed that a significant increase on the gene and proteins levels of nuclear factor erythroid 2-related factor 2 (NRF2, p < 0.05) and heme oxygenase-1 (HO-1, p < 0.05) have been observed in TCM-treated animals compared with that of in model animals. Interestingly, some indicators (serum MDA/SOD/TNF-α, RNA and protein levels of NRF2 and HO-1) showed more positive changes in TCM combined with western medicine (TCM-WN) - treated animals compared with that of TCM-treated animals.</p><p><strong>Conclusion: </strong>Modified Jinshui Liujian decoction and Bajitian pills effectively mitigate muscle atrophy associated with COPD by modulating the Nrf2/HO-1 pathway through multi-target mechanisms. The combined TCM and WM therapy demonstrates enhanced therapeutic efficacy compared to monotherapy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"66"},"PeriodicalIF":2.7,"publicationDate":"2025-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12012937/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144063621","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}
HereditasPub Date : 2025-04-17DOI: 10.1186/s41065-025-00426-3
Jing Sun, Shu Mei Tang, Jing Sun, Wei Gao
{"title":"Exploring the anticancer potential of green synthesized Zn/Cu nanocomposites from olive leaves against lung cancer.","authors":"Jing Sun, Shu Mei Tang, Jing Sun, Wei Gao","doi":"10.1186/s41065-025-00426-3","DOIUrl":"https://doi.org/10.1186/s41065-025-00426-3","url":null,"abstract":"<p><p>Lung cancer remains one of the leading causes of cancer-related death worldwide, with a significant number of patients succumbing to the disease each year. Olea europaea, commonly known as the olive tree, offers a range of health benefits due to its rich content of antioxidants. In the present study, we have reported the green synthesis of a bimetallic nanocomposite of zinc and copper using the leaf extract of Olea europaea (Zn/Cu NCs@ Olea europaea). The nanoparticles were characterized using common chemical techniques. The antioxidant activity of Zn/Cu NCs@ Olea europaea was evaluated using the DPPH assay. The cytotoxicity and anti-lung cancer activity of Zn/Cu NCs@ Olea europaea were investigated using the MTT assay. The results of XRD analysis and FE-SEM imaging showed a crystalline structure for Zn/Cu NCs@ Olea europaea with a semi-spherical morphology and an average size of 49.37 nm. Zn/Cu NCs@ Olea europaea scavenged the free radical DPPH with an IC<sub>50</sub> of 363.42 ± 5.02 µg/mL. Furthermore, Zn/Cu NCs@ Olea europaea exhibited acceptable anti-lung cancer activity by preventing growth in the cell lines SK-MES-1, A-549, and LK-2 with IC<sub>50</sub> of 154.00 ± 1.83, 228.83 ± 10.59, and 250.55 ± 8.04 µg/mL respectively. The NPs were inactive against the normal cell lines of HUVEC even at high concentrations. The results of the study indicate that Zn/Cu NCs@ Olea europaea, which is green synthesized with a sufficient nano size, can be considered a potent anti-lung cancer agent.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"65"},"PeriodicalIF":2.7,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12007358/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143969750","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}
HereditasPub Date : 2025-04-17DOI: 10.1186/s41065-025-00412-9
Peng Shen, Shunli Wu, Yi Chen, Guangjing Feng, Xue Guo, Yingguo Chen, Zhigang Wang, Youfeng Shen, Hongbo Wang, Ke Li
{"title":"Yi Gong San inhibits tumor immune escape by sensitizing colorectal cancer stem cells via the NF-κB pathway.","authors":"Peng Shen, Shunli Wu, Yi Chen, Guangjing Feng, Xue Guo, Yingguo Chen, Zhigang Wang, Youfeng Shen, Hongbo Wang, Ke Li","doi":"10.1186/s41065-025-00412-9","DOIUrl":"https://doi.org/10.1186/s41065-025-00412-9","url":null,"abstract":"<p><strong>Objective: </strong>Colorectal cancer (CRC), as a highly prevalent malignant tumor globally, faces the dual challenges of drug resistance of cancer stem cells and immune escape in its treatment. Although the traditional Chinese medicine Yigong San (YGS) shows potential in improving the clinical adverse reactions of CRC, its core active components and mechanism of action remain unclear. Based on network pharmacology screening, this study for the first time discovered that Gomisin B might regulate the progression of CRC through the Toll-like receptor 4/Nuclear Factor-kappa B (TLR4/NF-κB) signaling pathway, and aimed to systematically reveal the molecular mechanisms by which YGS and Gomisin B inhibited the malignant phenotypes and immune escape of CRC cells.</p><p><strong>Methods: </strong>The The Cancer Genome Atlas (TCGA) database was integrated with network pharmacology analysis to screen for the key target of CRC, Gomisin B, and its associated TLR4/NF-κB pathway. Through in vitro CRC stem cell models and mouse xenograft tumor models, techniques such as CCK-8, Transwell, flow cytometry, qPCR/WB were used to evaluate the effects of YGS and Gomisin B on proliferation, migration, invasion, apoptosis, and epithelial-mesenchymal transition (EMT), and to detect the expression of TLR4 and downstream inflammatory factors.</p><p><strong>Results: </strong>Both YGS and Gomisin B inhibited the proliferation, migration and invasion of CRC stem cells and tumor tissues. Meanwhile, they promoted apoptosis but reduced the expression of the inflammatory factor TLR4 and proteins associated with the NF-κB pathway, thereby exerting suppressive effects on tumorigenesis and disease progression. YGS might also impede EMT progression through modulation of the NF-κB pathway.</p><p><strong>Conclusion: </strong>This study for the first time elucidated the dual anti-tumor mechanisms of YGS, which sensitized CRC stem cells and inhibited immune escape by targeting the TLR4/NF-κB pathway through Gomisin B. It provides a pharmacological basis for the modern research of traditional Chinese medicine compound against CRC.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"64"},"PeriodicalIF":2.7,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143999207","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}
HereditasPub Date : 2025-04-16DOI: 10.1186/s41065-025-00383-x
Xiaotan Pan, Zhiyan Guo, Yin Zheng, Cheng Su, Jiabo Chen
{"title":"Effects of fourteen essential minerals and vitamins on acute and chronic tubulointerstitial nephritis: a multivariate Mendelian randomization study.","authors":"Xiaotan Pan, Zhiyan Guo, Yin Zheng, Cheng Su, Jiabo Chen","doi":"10.1186/s41065-025-00383-x","DOIUrl":"https://doi.org/10.1186/s41065-025-00383-x","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the causal relationship between minerals and vitamins and acute and chronic tubulointerstitial nephritis by Mendelian randomization.</p><p><strong>Methods: </strong>We selected fourteen minerals and vitamins from the GWAS database and acute tubulointerstitial nephritis and chronic tubulointerstitial nephritis from the Finnish database. Minerals and vitamins were first analyzed by two-sample Mendelian randomization for acute and chronic tubulointerstitial nephritis. The effects of minerals and vitamins on common acute and chronic tubulointerstitial nephritis were further explored by multivariate Mendelian randomization.</p><p><strong>Results: </strong>among fourteen minerals and vitamins by two-sample Mendelian randomization analysis, there was genetic causality for vitamin B6 and vitamin D on acute tubulointerstitial nephritis, and the results were vitamin B6 (β = -0.641; P = 0.049; OR = 0.527; 95% CI: 0.278-0.998); vitamin D (β = -3.165; P = 0.040; OR = 0.042; 95% CI: 0.002-0.861). Fourteen minerals and vitamins were not genetically causally associated with chronic tubulointerstitial nephritis. The presence of vitamin B6 was then analyzed by a multivariate Mendelian randomization study to independently affect acute tubulointerstitial nephritis and showed a negative correlation (P = 0.010; 95% CI: 0.021-0.159).</p><p><strong>Conclusion: </strong>We genetically predicted the possible influence of minerals and vitamins on acute and chronic tubulointerstitial nephritis. Vitamin B6 deficiency in vivo was found to adversely affect acute and chronic tubulointerstitial nephritis. This suggests that we pay clinical attention to the different effects that nutrients such as minerals and vitamins bring to acute and chronic tubulointerstitial nephritis.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"63"},"PeriodicalIF":2.7,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12004703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143983092","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}
HereditasPub Date : 2025-04-14DOI: 10.1186/s41065-025-00428-1
Guangming Li, Ying Guo, Yuanyuan Zhang
{"title":"Role of necroptosis and immune infiltration in essential thrombocytosis.","authors":"Guangming Li, Ying Guo, Yuanyuan Zhang","doi":"10.1186/s41065-025-00428-1","DOIUrl":"https://doi.org/10.1186/s41065-025-00428-1","url":null,"abstract":"<p><strong>Background: </strong>Necroptosis, a recently identified form of programmed cell death involved in the pathogenesis of a variety of tumor and non-tumor diseases. Nevertheless, the function of necroptosis in essential thrombocytosis (ET) remains unclear, which is a classic myeloproliferative tumor.</p><p><strong>Materials and methods: </strong>The role of necroptosis in ET was determined via bioinformatics combined with qRT-PCR analysis of clinical samples. GSE57793 and GSE26049 datasets were recruited to identify necroptosis differentially expressed genes based on differential gene identification, necroptosis gene sets and data machine learning. Enrichment analysis (GSEA) was used to evaluate the gene enrichment signaling pathway of ET, immune infiltration analysis was used to explore the abundance of immune cell infiltration in ET, and the correlation between necroptosis differential genes and immune cell infiltration was studied.</p><p><strong>Results: </strong>Five necroptosis genes were recognized to be remarkably enriched in the necroptosis pathway, including CHMP1B, FTH1, HSP90AB1, IL1A, and RBCK1. The imbalance of invasion of Th1/Th17 cells was identified in ET, and the differential necroptosis gene was positively correlated with the infiltration of multiple immune cells. There is significant necroptosis in ET, which is enriched in the necrotizing apoptotic pathway, and is associated with immune infiltration.</p><p><strong>Conclusions: </strong>Necroptosis might drive the progression of ET via stimulating immune infiltration and immune responses. The findings bring new insights into the treatment mechanism and treatment strategy of ET in the future.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"62"},"PeriodicalIF":2.7,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11995491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143994341","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":"E2F1-driven EXOSC10 transcription promotes hepatocellular carcinoma growth and stemness: a potential therapeutic target.","authors":"Haoyue Deng, Dingyong Wu, Yongpeng He, Xiaolei Yu, Jifei Liu, Yanrui Zhang, Bing Leng, Xiaofeng Yuan, Liguo Xiao","doi":"10.1186/s41065-025-00430-7","DOIUrl":"https://doi.org/10.1186/s41065-025-00430-7","url":null,"abstract":"<p><strong>Background: </strong>E2F Transcription Factor 1 (E2F1) is a transcription factor that plays a crucial role in the growth of many cancers, including hepatocellular carcinoma (HCC). Herein, this study probed the functions and underlying mechanisms of E2F1 in HCC tumorigenesis.</p><p><strong>Methods: </strong>The expression profiles of E2F1 and Exosome Component 10 (EXOSC10) were detected using qRT-PCR and western blotting. Functional experiments were carried out using 5-ethynyl-2'-deoxyuridine (EdU), flow cytometry, tube formation, and sphere formation assays in vitro, as well as xenograft experiments in vivo, respectively. Stemness-related proteins were assayed using western blotting. The interaction between E2F1 and EXOSC10 was verified using bioinformatics analysis and dual-luciferase reporter assay.</p><p><strong>Results: </strong>E2F1 was highly expressed in HCC tissues and cells, and was associated with advanced TNM stage, distant metastasis, and short survival rate. Functionally, knockdown of E2F1 suppressed HCC cell proliferation, angiogenesis, and stemness, and induced cell apoptosis. Mechanistically, E2F1 directly bound to the promoter region of EXOSC10 to up-regulate its expression. EXOSC10 silencing impaired HCC cell proliferation, angiogenesis, and stemness. Moreover, the anticancer effects of E2F1 knockdown were reversed by EXOSC10 elevation. In vivo assay, E2F1 deficiency suppressed HCC tumor growth and eliminated cancer stemness, while these effects were abolished by EXOSC10 up-regulation.</p><p><strong>Conclusion: </strong>E2F1 promotes EXOSC10 transcription and then facilitates HCC growth and cancer stemness, revealing a potential target for HCC therapy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"60"},"PeriodicalIF":2.7,"publicationDate":"2025-04-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11992873/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967761","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}