Hereditas最新文献

{"title":"Diagnostic value of LncRNA SNHG16 for osteoporotic fractures and its potential regulation of fracture healing.","authors":"Yuanming Luo, Qingfeng Zhang, Changqing Shao, Jin Li, Jiaojiao Chen, Liang Han, Xiaowei Jiang, Li Hong","doi":"10.1186/s41065-025-00423-6","DOIUrl":"https://doi.org/10.1186/s41065-025-00423-6","url":null,"abstract":"<p><strong>Background: </strong>Osteoporotic fractures (OPF) have a serious impact on the health of patients. It is of great importance to investigate the diagnostic effect of SNH16 on OPF and the mechanism of action to promote fracture healing.</p><p><strong>Methods: </strong>132 OPF patients and 128 OP patients were included. The levels of SNHG16, Col I, RUNX2 and OCN were evaluated by RT-qPCR. The diagnostic value of SNHG16 was evaluated by ROC curve. Cell proliferation ability was assessed by CCK-8, and apoptosis rate was detected by flow cytometry. ENCORI was used to predict the binding sites of SNHG16 with downstream target genes. DLR assay demonstrated the targeting relationship between SNHG16 and miR-432-5p.</p><p><strong>Results: </strong>SNHG16 was poorly expressed in OPF patients compared with OP patients, and its expression was lower in patients with delayed healing. In addition, in the OPF, OPG level was decreased, the level of RANKL was increased, and the balance of bone resorption formation is disrupted leading to fractures. Knockdown of SNHG16 results in decreased cell proliferation and increased apoptosis, and high SNHG16 expression decreases miR-432-5p expression, thereby increasing the levels of Col I, RUNX2 and OCN.</p><p><strong>Conclusion: </strong>Increasing SNHG16 can reduce the level of miR-432-5p thereby increasing the level of osteosynthesis proteins and restoring cellular activity, thereby promoting fracture healing.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"54"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803104","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of fatty acid metabolism-related genes in the tumor microenvironment of breast cancer by a development and validation of prognostic index signature.","authors":"Zhaofeng Ma, Man Zheng, Pulin Liu","doi":"10.1186/s41065-025-00425-4","DOIUrl":"https://doi.org/10.1186/s41065-025-00425-4","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer (BRCA) is a malignancy originating in the breast cells, characterized by a poor overall survival rate. Post-resection, chemotherapy is commonly recommended as a primary therapeutic approach; however, its efficacy remains limited. Recent advancements in lipidomics and metabolomics have provided new insights into the intricate landscape of fatty acid metabolism (FAM) and the fatty acid lipidome in both health and disease. A growing body of evidence suggests that dysregulations in FAM and fatty acid levels play a significant role in cancer initiation and progression. Despite these advances, the precise mechanisms through which FAM mediates the anti-cancer effects of lobaplatin in BRCA remain poorly understood and warrant further investigation.</p><p><strong>Methods: </strong>GEO and TCGA data were classified into two types. We aimed to show how FAMGs influence immune function, immune checkpoints, and m6a in BRCA. A co-expression analysis discovered that gene expression is strongly connected to pyroptosis. The TCGA gathered information about mRNAsi, gene mutations, CNV, and clinical features.</p><p><strong>Results: </strong>In the low-risk group, overall survival (OS) is longer. GSEA was utilized to identify immune and tumor-related pathways. Most of the FAMG-derived prognostic signatures predominantly modulate immunological and oncogenic signaling pathways, including the Wnt, neurotrophin, chemokine, and calcium signaling cascades. Among the genes involved are CEL, WT1, and ULBP2. Expression levels varied as well. The prognostic model, CNVs, single nucleotide polymorphism (SNP), and drug sensitivity all pointed to the gene.</p><p><strong>Conclusions: </strong>The primary objective of this study is to identify and validate BRCA-associated FAMGs that can serve as prognostic indicators and provide insights into immune system function, while also offering evidence to support the development of fatty acid metabolism-related molecularly targeted therapeutics. Consequently, FAMGs and their interactions with the immune system, as well as their role in BRCA, may emerge as promising therapeutic targets.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"55"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of bioinformatics analysis and molecular docking to study the mechanism of Qingying decoction in treating psoriasis.","authors":"Cuicui Shen, Xuewei Liu, Huangchao Jia, Wenhe Wang, Xiaomeng Wang, Haiyan Wang, Dan Wang, Jianwei Li","doi":"10.1186/s41065-025-00421-8","DOIUrl":"https://doi.org/10.1186/s41065-025-00421-8","url":null,"abstract":"<p><strong>Background: </strong>Qingying decoction (QYD) is a traditional prescription in China that has been shown to be effective in treating psoriasis. However, its mechanism of action remains to be elucidated.</p><p><strong>Methods: </strong>The active ingredients and targets of QYD were obtained from TCMSP database, HERB database and SwissTargetPrediction database, respectively. Differential expression gene (DEGs) analysis and weighted gene co-expression network analysis (WGCNA) were used to identify key genes associated with psoriasis. Protein-protein interaction (PPI) network was constructed using STRING platform. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using the DAVID database and the clusterProfiler package of R software. Cytoscape 3.9.0 software was used to screen the key components of QYD and the hub targets. Molecular docking was used to detect the binding ability between key components and hub targets. An in vitro model of psoriasis was established by stimulating keratinocyte HaCaT with a mixture of five pro-inflammatory cytokines (IL-17 A, IL-22, IL-1α, oncostatin M, and TNF-α) (M5). Cell viability and cell cycle were measured using cell counting Kit 8 (CCK-8) and flow cytometry, respectively. Real-time quantitative polymerase chain reaction (qRT-PCR) was used to detect mRNA levels of hub genes, high-proliferation marker keratin 6 (KRT6) and inflammatory factors IL-1β, IL-6 and TNF-α. Protein expression levels of PI3K/AKT/FoxO pathway related targets were detected by Western blot.</p><p><strong>Results: </strong>A total of 139 active ingredients of QYD were screened in this study, with 1033 targets, 59 of which overlapped with psoriasis-related genes. Quercetin, luteolin, kaempferol, beta-sitosterol and methylophiopogonanone A were considered to be the key ingredients of QYD in the treatment of psoriasis. CDC25A, TOP2A, NEK2 and CCNA2 were identified to be the hub targets. QYD could probably regulate cell cycle, T cell receptor signaling pathway and metabolic pathway to treat psoriasis. The key components of QYD had good binding affinity with hub target proteins. QYD significantly attenuated M5-induced hyperproliferation and cell cycle progression of HaCaT cells. M5 stimulation significantly upregulates the mRNA levels of CDC25A, TOP2A, NEK2, CCNA2, IL-1β, IL-6 and TNF-α, while QYD treatment reversed this effect. In addition, QYD treatment inhibited the phosphorylation of PI3K and AKT in M5-stimulated HaCaT cells and upregulated p-FOXO1 protein expression level.</p><p><strong>Conclusion: </strong>QYD can inhibit the excessive proliferation and inflammatory response of keratinocytes by regulating the PI3K/AKT/FoxO pathway, suggesting that QYD may be an attractive prescription for psoriasis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"52"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of lncRNAs in peripheral blood mononuclear cells associated with sepsis immunosuppression based on weighted gene co-expression network analysis.","authors":"Wenjia Zhang, Yan Li, Gang Li, Aijia Zhang, Wende Sun","doi":"10.1186/s41065-025-00400-z","DOIUrl":"10.1186/s41065-025-00400-z","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-induced immunosuppression involves complex molecular mechanisms, including dysregulated long noncoding RNAs (lncRNAs), which remain poorly understood.</p><p><strong>Objective: </strong>We aimed to identify immunosuppression-related lncRNAs and their functional pathways in sepsis. Methods: Using weighted gene coexpression network analysis (WGCNA), we analyzed lncRNA profiles from peripheral blood mononuclear cells (PBMCs) of three sepsis patients and three healthy controls. Key modules linked to immunosuppression were validated via RT-PCR and external datasets. Pathway enrichment and protein interaction networks were employed to prioritize mechanisms.</p><p><strong>Results: </strong>A sepsis-associated module containing 4,193 lncRNAs revealed three immunosuppression-related pathways: Th17 cell differentiation, cytokine-cytokine receptor interactions, and cancer-related proteoglycan signaling. Protein-protein interaction networks identified three central genes (SLFN12, ICOS, IKZF2) and their linked lncRNAs (ENSG00000267074, lnc-ICOSLG-1, lnc-IKZF2-7), all significantly downregulated in sepsis patients.</p><p><strong>Conclusion: </strong> Our findings highlight novel lncRNA-regulated pathways in sepsis-induced immunosuppression, providing potential targets for improved diagnosis and therapy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"51"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of N6-methyladenosine-associated ferroptosis biomarkers in cervical cancer.","authors":"Jinzhe Liu, Buwei Han, Xijiao Hu, Mengke Yuan, Zhiwei Liu","doi":"10.1186/s41065-025-00418-3","DOIUrl":"https://doi.org/10.1186/s41065-025-00418-3","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer (CC) stands as a major contributor to female mortality. The pathogenesis of CC is linked with various factors. Our research aimed to unravel the underlying mechanisms of ferroptosis and m6A RNA methylation in CC through bioinformatics analysis.</p><p><strong>Methods: </strong>Three CC datasets, including GSE9750, GSE63514, and TCGA-CESC, were incorporated. m6A-related genes were derived from published sources, while ferroptosis-related genes were obtained from the FerrDb database. Differential expression and correlation analyses were performed to identify differentially expressed m6A-related ferroptosis genes (DE-MRFGs) in CC. Subsequently, the biomarkers were further identified using machine learning techniques. Gene Set Enrichment Analysis (GSEA) and Kaplan-Meier (KM) survival analysis were also performed to comprehend these biomarkers. Furthermore, a competing endogenous RNAs (ceRNA) network involving biomarkers was established. Finally, biomarkers expression were verified by real-time quantitative polymerase chain reaction (RT-qPCR).</p><p><strong>Results: </strong>From the DE-MRFGs, six genes, including ALOX12, EZH2, CA9, CDCA3, CDC25A, HSPB1, were selected. A nomogram constructed based on these biomarkers exhibited potential clinical diagnostic value for CC, with good diagnostic accuracy confirmed through calibration curves. GSEA unveiled associations of these biomarkers with cell proliferation, spliceosome, and base excision repair. KM survival analysis demonstrated significant differences in survival outcomes between high and low expressions of HSPB1, EZH2, and CA9 samples. A ceRNA network was constructed involving three biomarkers, such as CDC25A, CDCA3, and EZH2, 29 miRNAs, and 25 lncRNAs. In RT-qPCR verification, the expression of ALOX12, EZH2 and CDC25A was significantly higher in CC samples, while HSPB1 expression was higher in control samples.</p><p><strong>Conclusion: </strong>Six genes, namely ALOX12, EZH2, CA9, CDCA3, CDC25A, and HSPB1, were identified as m6A-regulated ferroptosis biomarkers in CC. These findings offer valuable insights into disease pathogenesis and hold promise for advancing CC treatment and prognosis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"53"},"PeriodicalIF":2.7,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification and validation of CDC20 and ITCH as ubiquitination related biomarker in idiopathic pulmonary fibrosis.","authors":"Shulei Sun, Yubao Wang, Jing Feng","doi":"10.1186/s41065-025-00401-y","DOIUrl":"10.1186/s41065-025-00401-y","url":null,"abstract":"<p><strong>Purpose: </strong>Ubiquitination plays a crucial role in various diseases. This study aims to explore the potential ubiquitination related genes in IPF.</p><p><strong>Methods: </strong>The gene microarray dataset GSE24206 was obtained from GEO database. Subsequently, through differential expression analysis and molecular signatures database, we obtained 1734 differentially expressed genes and 742 ubiquitination related genes. Through the venn diagram analysis, we obtained 53 differentially expressed ubiquitination related genes. Then, gene-ontology (GO) enrichment analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, protein-protein interactions (PPI) and gene set enrichment analysis (GSEA) were applied for the differentially expressed ubiquitination related genes. Finally, the expression of CDC20 and ITCH in IPF patients and cells were validated by qPCR and western blot assay.</p><p><strong>Results: </strong>A total of 53 differentially expressed ubiquitination related genes (36 up-regulated genes and 17 down-regulated genes) were identified between 17 IPF patients and 6 healthy controls. GO and KEGG enrichment analysis of ubiquitination related genes mainly involved in regulation of protein ubiquitination, regulation of post-translational protein modification and ubiquitin mediated proteolysis. The PPI results demonstrated that these ubiquitination related genes interacted with each other. The GSEA analysis results for some of the hub genes mainly involved epithelial mesenchymal transition, inflammatory response, hypoxia, and apoptosis. The experiment expression level of CDC20 and ITCH in IPF patients and IPF cells were consistent with the bioinformatics analysis results.</p><p><strong>Conclusion: </strong>We identified 53 potential ubiquitination related genes of IPF through bioinformatics analysis. CDC20 and ITCH and other ubiquitination related genes may influence the development of IPF through epithelial mesenchymal transition and inflammatory response. Our research findings provide insights into the mechanisms of fibrosis and may provide evidence for potential therapeutic targets for fibrosis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"50"},"PeriodicalIF":2.7,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11959808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143763892","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":"Characterization of key genes and immune cell infiltration associated with endometriosis through integrating bioinformatics and experimental analyses.","authors":"Ying Peng, Xiangdong She, Ying Peng","doi":"10.1186/s41065-025-00417-4","DOIUrl":"10.1186/s41065-025-00417-4","url":null,"abstract":"<p><strong>Backgrounds: </strong>Endometriosis (EM) is the most common gynecological disease in women of childbearing age. This study aims to identify key genes and screen drugs that may contribute to EM treatment.</p><p><strong>Methods: </strong>The differentially expressed genes (DEGs) were identified using limma analysis in the GSE11691 dataset. The protein-protein network (PPI) was constructed. Four machine learning methods, including LASSO, SVM-RFE, random forest, and Boruta, were applied to identify the key genes associated with EM. Flow cytometry, wound healing, and migration assays were applied to assess the cell functions of APLNR on hEM15A. The immune cell infiltration of each sample in EM was calculated using a single-sample gene set enrichment analysis (ssGSEA) algorithm. The potential drugs were screened using the Connectivity Map (CMAP) database, based on the DEGs. Finally, the expression levels of the three genes were further validated in the GSE23339 dataset.</p><p><strong>Results: </strong>One hundred thirty-seven down-regulated genes and 304 up-regulated genes were identified. We identified three key genes associated with EM: APLNR, HLA-DPA1, and AP1S2. The ssGSEA analysis results indicated that these genes play an important role in the development of EM. Moreover, EM immune cell infiltration was tightly associated with these three genes. Finally, several molecular compounds targeting EM were screened with the connectivity map (CMAP) database. ShAPLNR decreased the cell viability of hEM15A, increased the number of apoptotic cells, and significantly decreased the proportion of callus through APLNR in vitro studies.</p><p><strong>Discussion: </strong>Three genes (APLNR, HLA-DPA1, and AP1S2) may serve as novel therapeutic targets for diagnosing and treating patients with EM.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"49"},"PeriodicalIF":2.7,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11956255/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752387","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":"Infiltrating B-cell subtypes and associated hub genes in nasopharyngeal carcinoma identified from integrated single-cell, bulk RNA-sequencing, and immunohistochemical data.","authors":"Fangyan Zhong, Junjun Chen, Tianzhu Lu, Lin Zhang, Zhiliang Liu, Chunhong Guan, Xiaopeng Xiong, Xiaochang Gong, Jingao Li","doi":"10.1186/s41065-025-00414-7","DOIUrl":"10.1186/s41065-025-00414-7","url":null,"abstract":"<p><strong>Background: </strong>Nasopharyngeal carcinoma (NPC) is associated with lymphocyte infiltration; however, the majority of research on NPC has focused on the role of T cells, with relatively little known about the roles of B cells and their subtypes. Therefore, we evaluated the prognostic value of CD20 + B cell density and B-cell subtypes along with their functional enrichment and hub genes in NPC.</p><p><strong>Methods: </strong>The prognostic value of CD20 + B-cell density for distant metastasis-free survival (DMFS), overall survival (OS), and progression-free survival (PFS) was explored by immunohistochemistry using multivariate analysis. Transcriptomic expression data from Gene Expression Omnibus (GEO) datasets were analyzed to identify B-cell subtypes and their functional enrichment in NPC tissues. Pseudotime trajectory analysis was performed to evaluate the B-cell differentiation trajectory and hub genes were identified using Cytoscape software.</p><p><strong>Results: </strong>Patients with NPC exhibiting a high infiltrating density of CD20⁺ B cells showed significantly better 5-year DMFS, OS, and PFS compared to those of patients with a low infiltrating density. Naïve B cells, switched memory B cells, exhausted B cells, and plasma cells were identified as key B-cell subtypes infiltrating NPC tumors, with naïve B cells showing the highest infiltration levels associated with a better prognosis. Naïve B cells were closely associated with immune pathways and the hub genes were typical markers for T and B cells.</p><p><strong>Conclusion: </strong>A high infiltrating density of B cells showed strong prognostic value in patients with NPC. Naïve B cells may play an important role in tumor immunity for NPC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"48"},"PeriodicalIF":2.7,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954199/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742667","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":"Activation of TRIM37 by ATF6 and degradation of ACSL4: inhibiting ferroptosis and propelling cervical cancer progression.","authors":"Yang Wang, Li Xie, Shiying Jin, YouXiang Hou, Yina Wang","doi":"10.1186/s41065-025-00404-9","DOIUrl":"10.1186/s41065-025-00404-9","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer (CC), a prevalent gynecological malignancy, shows high global incidence and mortality. Tripartite motif-containing 37 (TRIM37), a significant ubiquitinating enzyme, is overexpressed in CC, fueling its progression, but its role in ferroptosis here is unknown.</p><p><strong>Methods: </strong>TRIM37 expression in CC tissues was first predicted using bioinformatics software. Then, RT-qPCR and Western blot were utilized to confirm TRIM37 expression in CC tissues and cells. Subsequently, cellular behaviors were examined by EdU, flow cytometry, and Transwell assay. Besides, ferroptosis-related indicators were detected by using corresponding kits. The dual luciferase reporter assay was conducted to identify the binding between TRIM37 and Activating Transcription Factor 6 (ATF6). Additionally, the Co-IP assay was applied to validate the interaction between TRIM37 and Acyl-CoA Synthetase Long-Chain Family Member 4 (ACSL4). Finally, the functions of TRIM37 in vivo were investigated by establishing a xenograft tumor model.</p><p><strong>Results: </strong>TRIM37 expression was increased in CC tissues and cells. Silencing TRIM37 suppressed cell malignant behaviors and promoted ferroptosis. ATF6 activated TRIM37 transcription, with TRIM37 upregulation counteracting ATF6 knockdown effects. TRIM37 degraded ACSL4, and silencing ACSL4 reversed TRIM37 knockdown effects. TRIM37 overexpression counteracted ATF6 knockdown's impact on tumor growth in vivo.</p><p><strong>Conclusion: </strong>ATF6 regulated the expression of TRIM37, which in turn promoted the ubiquitination and degradation of ACSL4, facilitating the progression of CC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"47"},"PeriodicalIF":2.7,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11954333/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742576","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":"A bioinformatics analysis of the target role of miRNA-431-5p on KLK6 in colorectal cancer.","authors":"Juan Wang, Zonglang Lai, Na Liu, Yuhong Wang, Feng Li, Na Song, Jun Cheng","doi":"10.1186/s41065-025-00395-7","DOIUrl":"https://doi.org/10.1186/s41065-025-00395-7","url":null,"abstract":"<p><strong>Background: </strong>Although increasing evidence suggests that microRNAs (miRNAs) play different roles in the occurrence, development, and prognosis of colorectal cancer (CRC), investigations on miRNA-targeted regulation in CRC are sparse. However, the high morbidity and mortality of CRC necessitates exploring this area of research for potential alternative therapeutic approaches to CRC.</p><p><strong>Methods: </strong>Bioinformatics analysis was used to obtain the key Hub genes related to CRC, and survival analysis was performed to screen out the core genes. Meanwhile, verification was performed using CCK-8, Transwell, qPCR, WB, immunohistochemistry and dual luciferase assays at a cellular level.</p><p><strong>Results: </strong>This study identified the hub gene KLK6 associated with CRC based on the GEO and TCGA databases. Survival analysis revealed a significant decrease in the survival rate of CRC patients with increasing expression levels of KLK6. Target gene prediction confirmed that miR-431-5p can target KLK6. Cell experimental results demonstrated that the miR-431-5p inhibitor enhanced cell viability and promoted cell migration and invasion while miR-431-5p mimics reduced cell viability and inhibited cell migration and invasion. Both the inhibitor and mimics of miR-431-5p suppressed and promoted the expression of miR-431-5p, as well as promoted and inhibited the KLK6 mRNA and protein expression. Dual luciferase results showed that miR-431-5p targeted KLK6, and cell recovery experiments further verified that miR-431-5p regulated cell viability, migration and invasion by targeting KLK6.</p><p><strong>Conclusions: </strong>Through target gene prediction, miR-431-5p was found to target KLK6, suggesting its therapeutic potential in CRC. As such, therapies that can inhibit KLK6 via miR-431-5p offer a promising approach to CRC.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"46"},"PeriodicalIF":2.7,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11951700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742379","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}