Hereditas最新文献

{"title":"Beyond the variant: hereditary cancer awareness in the multi-omics era.","authors":"Julhash U Kazi, Ramin Massoumi","doi":"10.1186/s41065-026-00738-y","DOIUrl":"10.1186/s41065-026-00738-y","url":null,"abstract":"<p><p>Hereditary cancer awareness has entered a new phase. For decades, awareness has focused on recognizing familial risk, identifying pathogenic germline variants, and helping families access counselling, surveillance and prevention. Yet in 2026, the main challenge is no longer only whether a variant can be detected, but how inherited risk can be interpreted, communicated and translated into action in the biological context of each tissue and tumor. The recent publication landscape of Hereditas illustrates this shift: cancer genetics is now inseparable from RNA regulation, epigenetics, metabolism, immune context, cellular plasticity, therapy resistance, computational modelling and precision intervention. This Editorial argues that hereditary cancer awareness must move beyond the variant without moving away from the familial risk. One step in this direction could be to use multi-omics as a bridge between genetic risk and precision prevention.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621766/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074512","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":"Hereditary breast cancer: emerging roles of non-coding RNAs.","authors":"Zhenshan Yang, Dipanjan Guha, Ling Zhang, Honglu Diao, Angshuman Bagchi","doi":"10.1186/s41065-026-00720-8","DOIUrl":"10.1186/s41065-026-00720-8","url":null,"abstract":"<p><p>Breast cancer remains a major global health burden and is characterized by substantial molecular and clinical heterogeneity. In recent years, considerable progress has been made in elucidating the genetic and molecular mechanisms underlying breast cancer, particularly those associated with hereditary susceptibility. Advances in genomic and functional studies have further revealed the complex mutational landscape of breast cancer, including key alterations in tumor suppressor genes, oncogenic signaling pathways, and mutagenic processes. In addition, non-coding RNAs (ncRNAs) have emerged as important regulators of gene expression, influencing tumor progression and therapeutic resistance. Emerging strategies, including immunotherapy, precision medicine, and nanoparticle-based drug delivery systems, have significantly expanded treatment options and improved clinical outcomes. However, challenges such as tumor heterogeneity, drug resistance, systemic toxicity, and disparities in healthcare access continue to limit the effectiveness and broad implementation of these therapies. This review provides a comprehensive overview of the molecular mechanisms of breast cancer from a hereditary perspective, with a particular focus on genetic susceptibility, ncRNAs, and emerging therapeutic strategies. Additionally, it highlights current limitations and future directions, emphasizing the need for integrative approaches that combine genomic insights, advanced technologies, and personalized medicine to improve breast cancer prevention and treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617922/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149069441","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 mapping of TIMP1-associated stromal-myeloid remodeling in autoimmune gastritis and gastric cancer.","authors":"Jialiang Cai, Jie Li, Shu Tian, Ning Yang, Yi Wang, Xinmin Li, Yi Zhang, Shulian Bai","doi":"10.1186/s41065-026-00736-0","DOIUrl":"10.1186/s41065-026-00736-0","url":null,"abstract":"<p><strong>Background: </strong>Autoimmune gastritis (AIG) is a chronic immune-mediated atrophic disease that can induce cancer-related epithelial remodeling, although its association with gastric adenocarcinoma depends on histological and clinical modifiers. Gastric cancer (GC) progression is shaped by the tumor microenvironment (TME), including cancer-associated fibroblasts (CAFs), myeloid cells, and extracellular matrix (ECM) remodeling. Whether AIG-related mucosal remodeling shares stromal programs with GC-associated stromal-myeloid niches remains unclear.</p><p><strong>Methods: </strong>We integrated one AIG bulk-transcriptomic cohort and three GC cohorts to identify shared differentially expressed genes (DEGs), followed by LASSO, random forest and protein-protein interaction (PPI) analyses. TIMP1 was evaluated using tissue transcriptomic cohorts, serum RT-qPCR, survival analysis, immune infiltration profiling, scRNA-seq, inferCNV-based epithelial classification, CellChat ligand-receptor inference and spatial transcriptomics.</p><p><strong>Results: </strong>A total of 51 shared DEGs were identified between AIG and GC. TIMP1 was the only candidate supported by both machine-learning screening and PPI hub-gene analysis. TIMP1 was upregulated in GC tissues and serum and showed an exploratory tumor-normal ROC AUC of 0.941 in the TCGA_STAD cohort, while higher TIMP1 expression was associated with poorer overall survival. Functional analyses linked TIMP1-high GC to ECM organization, integrin binding, epithelial-mesenchymal transition (EMT), transforming growth factor-β signaling and immune infiltration. scRNA-seq of 160,812 GC cells localized TIMP1 mainly to CAF and myeloid compartments. In AIG, TIMP1-high fibroblasts displayed enhanced CAF-associated stromal and inflammatory transcriptional programs. CellChat and spatial transcriptomics further linked TIMP1-associated stromal and myeloid states to ECM-dominant communication and fibroblast-rich, myeloid-associated remodeling regions.</p><p><strong>Conclusions: </strong>TIMP1 may mark related stromal-myeloid remodeling states across AIG-associated mucosal remodeling and GC, providing a hypothesis-generating framework potentially relevant to inflammation-associated gastric tumorigenesis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13617772/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074488","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":"Diagnostic and mechanistic roles of miR-5584-5p in endometriosis via the FZD2-mediated Wnt/β-catenin EMT axis.","authors":"Wandi Zhang, Min Zhang, Han Lu, Wanli Ji","doi":"10.1186/s41065-026-00732-4","DOIUrl":"https://doi.org/10.1186/s41065-026-00732-4","url":null,"abstract":"<p><strong>Background: </strong>The early detection of endometriosis (EM), a significant cause of dysmenorrhea, is essential for effective clinical management. This study sought to determine the functional role of miR-5584-5p in EM and the mechanistic involvement of its target, FZD2, in disease progression.</p><p><strong>Methods: </strong>This case-control study enrolled 217 dysmenorrhea patients (107 EM cases and 110 controls). Ishikawa cells with modulated miR-5584-5p and FZD2 expression were used to assess cell proliferation, migration, and invasion. The miR-5584-5p/FZD2 interaction and Wnt/β-catenin transcriptional activity were validated by dual-luciferase and TOP/FOP flash reporter assays.</p><p><strong>Results: </strong>Serum miR-5584-5p was significantly downregulated in EM patients, demonstrating high diagnostic accuracy (AUC = 0.903) and acting as an independent protective factor. In vitro, miR-5584-5p overexpression suppressed Ishikawa cell proliferation, migration, and invasion, concurrently inhibiting Wnt/β-catenin transcriptional activity and the epithelial-mesenchymal transition (EMT) axis. FZD2 was confirmed as a direct target of miR-5584-5p. Crucially, FZD2 overexpression partially reversed the inhibitory effects of miR-5584-5p on malignant cellular phenotypes and restored Wnt/β-catenin signaling.</p><p><strong>Conclusion: </strong>Serum miR-5584-5p serves as a valuable potential diagnostic biomarker for EM. Functionally, it attenuates endometrial epithelial cell aggressiveness by targeting FZD2 and suppressing the Wnt/β-catenin-EMT axis. Future studies utilizing primary cells and in vivo models are warranted to validate these preliminary mechanisms.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13628742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149108892","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":"Haplotype-based validation of genomic regions for breeding of new Nordic apples.","authors":"Jonas Skytte Af Sätra, Dag Røen, Tuuli Haikonen, Kimmo Rumpunen, Larisa Garkava-Gustavsson, Stein Harald Hjeltnes","doi":"10.1186/s41065-026-00728-0","DOIUrl":"https://doi.org/10.1186/s41065-026-00728-0","url":null,"abstract":"<p><p>When breeding apple cultivars for northern latitudes, early harvest and late flowering are desirable to manage the short growing season and ongoing climatic changes. Depending on the intended use, increased content of polyphenolic compound might be considered desirable (juice and cider) or undesirable (dessert). Thus, we phenotyped a total of 111, 189, and 88 apple genotypes for harvest date, flowering date, and peel concentration of procyanidin B2 (PRB2), respectively, across three Nordic locations in Sweden, Norway, and Finland. Using phased marker data from the 20 K apple Infinium^® SNP array we performed haplotype-based validation of previously described quantitative trait loci (QTL) intervals and genomic regions on Linkage Group (LG) 3 (harvest date), LG 9 and 12 (flowering), and LG16 (PRB2). We assessed the correlation between the traits and historical climate adaptation and identified haplotypes associated with increasing and decreasing effects for the three traits. These results are valuable for Marker Assisted Parent Selection in the Nordic breeding programs, as they support designing crosses to meet the demands of current and future climatic conditions, and fruit quality towards breeding of new dessert cultivars, or cultivars for juice or cider production.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13474611/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148760019","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 prognostic value of miR-363-5p in colorectal cancer and its associated molecular mechanisms.","authors":"Feng Xue, Yuanguo Si, Zhuoli Gao, Peng Hou","doi":"10.1186/s41065-026-00716-4","DOIUrl":"10.1186/s41065-026-00716-4","url":null,"abstract":"<p><strong>Background: </strong>Colorectal cancer (CRC) is a prevalent malignant neoplasm characterized by high incidence and mortality rates. Currently, the role of microRNAs (miRNAs) in CRC is increasingly recognized. In this study, we aim to investigate the prognostic value of miR-363-5p and its associated molecular mechanisms.</p><p><strong>Methods: </strong>A total of 156 paired samples were collected from patients with CRC. The levels of miR-363-5p in the samples were detected by RT-qPCR. KM curves and multivariable Cox regression models evaluated the prognostic value of miR-363-5p. Flow cytometry, CCK-8 assay and Transwell assay examined the effects of miR-363-5p on cellular malignant phenotypes. Dual-luciferase reporter assays validated the targeting relationship.</p><p><strong>Results: </strong>The expression level of miR-363-5p was declined in CRC, and patients with TNM stage III + IV exhibited lower miR-363-5p expression compared to those with TNM stage I + II. Furthermore, individuals with low miR-363-5p expression demonstrated shorter overall survival than those with high expression, and miR-363-5p was confirmed as an independent protective factor for CRC. In vitro, miR-363-5p suppressed cellular malignant phenotypes, primarily manifested by miR-363-5p mimic promoting apoptosis while inhibiting proliferation, migration and invasion. Mechanistically, we identified MEIS3 as a direct target of miR-363-5p, and rescue experiments confirmed that MEIS3 overexpression attenuated the tumor-suppressive effects of miR-363-5p.</p><p><strong>Conclusions: </strong>Downregulated miR-363-5p were involved in CRC progression and associated with poor patient prognosis. Mechanistically, upregulated miR-363-5p suppressed the malignant cellular phenotype by negatively regulating MEIS3, thereby inhibiting the progression of CRC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13584593/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148989790","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":"MicroRNA-345-3p expression inhibits colorectal cancer liver metastasis by targeting KHDRBS1 and TGF-β signaling pathway.","authors":"Song Fan, Jian Zhao, Songjie Liu, Bing Xu, Xiangting Cheng","doi":"10.1186/s41065-026-00715-5","DOIUrl":"10.1186/s41065-026-00715-5","url":null,"abstract":"<p><strong>Objective: </strong>The aim of this study was to investigate the association of microRNA-345-3p (miR-345-3p) with liver metastasis in colorectal cancer (CRC) and to explore its underlying molecular mechanisms using in vitro approaches.</p><p><strong>Methods: </strong>Serum specimens were collected from 110 CRC patients and 90 healthy individuals. Quantitative real-time PCR (qRT-PCR) was employed to assess the expression levels of miR-345-3p and KH RNA binding domain containing, signal transduction associated 1 (KHDRBS1) expression. The associations of miR-345-3p with clinical pathological characteristics, survival, and liver metastasis were analyzed. In vitro cell experiments were conducted to validate the effects of miR-345-3p on CRC cell growth and epithelial-mesenchymal transition (EMT). Target genes and signaling pathways were verified using luciferase reporter assays, rescue experiments, and Western blot analysis.</p><p><strong>Results: </strong>A significant decrease in miR-345-3p expression was observed in CRC patients with liver metastasis. Low levels of miR-345-3p were correlated with advanced tumor node metastasis (TNM) stages, deeper invasion, lymph node metastasis, and poorer prognosis. Overexpression of miR-345-3p inhibited CRC cell growth and suppressed EMT-associated molecular changes. Bioinformatics analyses and experimental results confirmed KHDRBS1 as a direct target gene of miR-345-3p. Furthermore, rescue experiments demonstrated that overexpression of KHDRBS1 reverses the tumor-suppressive effects of miR-345-3p, indicating that miR-345-3p functions by regulating the transforming growth factor-β (TGF-β) signaling pathway.</p><p><strong>Conclusions: </strong>Decreased circulating levels of miR-345-3p are associated with liver metastasis in CRC. In vitro studies suggest that miR-345-3p may exert its tumor-suppressive effects by targeting KHDRBS1 and suppressing the TGF-β signaling pathway, thereby inhibiting CRC cell migration and invasive capacity.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13560245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148929592","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":"Targeting RASL12 by miR-6791-5p fuels malignant progression in lung adenocarcinoma.","authors":"Lu Zhang, Zhonghao Pang, Haibo Zhang, Pin Wang","doi":"10.1186/s41065-026-00697-4","DOIUrl":"https://doi.org/10.1186/s41065-026-00697-4","url":null,"abstract":"<p><strong>Background: </strong>Lung adenocarcinoma (LUAD) poses significant clinical challenges due to its heterogeneity and metastatic potential, necessitating deeper molecular characterization. This study investigated the role of miR-6791-5p and its target RASL12 in LUAD progression.</p><p><strong>Methods: </strong>Expression profiles and prognostic relevance were analyzed in 203 LUAD patients, cell lines, and public databases. Biological functions were evaluated through CCK-8, Transwell, independent RASL12 knockdown, and rescue assays. Interactions were validated by dual-luciferase assays. Downstream pathways were explored via Gene Set Enrichment Analysis (GSEA).</p><p><strong>Results: </strong>miR-6791-5p was significantly upregulated in LUAD (p < 0.001), independently predicting poor overall survival (HR = 2.411, p = 0.003). Functionally, miR-6791-5p promoted LUAD cell proliferation, migration, and invasion. RASL12 was confirmed as a direct target, exhibiting decreased mRNA and protein expression in tumors that negatively correlated with miR-6791-5p. Independent RASL12 knockdown enhanced tumor aggressiveness, while its co-knockdown partially reversed the tumor-suppressive effects of miR-6791-5p inhibition. GSEA linked this axis to cell adhesion signaling dynamics.</p><p><strong>Conclusions: </strong>miR-6791-5p acts as an oncogene in LUAD by directly targeting the tumor suppressor RASL12. This axis modulates malignant phenotypes, representing a promising prognostic biomarker and potential therapeutic candidate.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13491930/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148792177","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":"miR-335-3p acts as a tumor suppressor in esophageal squamous cell carcinoma and predicts favorable prognosis.","authors":"Miao He, Shuojun Lu, Feng Yang, Jiangqi Xu, Ran Zhu","doi":"10.1186/s41065-026-00702-w","DOIUrl":"10.1186/s41065-026-00702-w","url":null,"abstract":"<p><strong>Background: </strong>Esophageal cancer is a highly invasive malignancy that severely impairs normal digestive function and poses a substantial threat to patient survival. The pathogenesis of miRNA-mediated tumors has been widely documented.</p><p><strong>Aim: </strong>Verifying the involvement of miR-335-3p in the pathogenesis of esophageal squamous cell carcinoma (ESCC).</p><p><strong>Methods: </strong>The study enrolled 90 ESCC patients, from whom clinical data and pathological tissue samples were acquired. The prognostic potential of dysregulated miR-335-3p in ESCC was assessed using the Kaplan-Meier method. miR-335-3p and GFPT1 expression in the specimens were measured by RT-qPCR. Cellular biological functions were verified through transfection, CCK-8, Transwell, and kit-based assays. The targeting relationship was ascertained by luciferase activity assays.</p><p><strong>Results: </strong>miR-335-3p was downregulated in ESCC, which is indicative of poorer prognostic outcomes. GFPT1 was up-regulated and was regarded as a target of miR-335-3p. Increased miR-335-3p levels markedly impaired cellular biological functions. Conversely, simultaneous overexpression of GFPT1 alleviated the negative effects induced by miR-335-3p mimic, which was associated with the partial restoration of cell activity and antioxidant capacity.</p><p><strong>Conclusion: </strong>miR-335-3p represents a potential independent prognostic marker in ESCC. The anti-tumor activity induced by miR-335-3p overexpression may be associated with its regulation of GFPT1.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148548695","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":"SNP rs7430456 mediated LINC00578 drives triple negative breast cancer through regulating miR-143-5p expression.","authors":"Jing Zhai, Wei Wu, Xiaoyun Mao, Lianjun Wu","doi":"10.1186/s41065-026-00705-7","DOIUrl":"10.1186/s41065-026-00705-7","url":null,"abstract":"<p><strong>Background: </strong>A large number of cancer-related single-nucleotide polymorphisms (SNPs) are distributed in the genomic regions of long non-coding RNAs (lncRNAs), yet the mechanisms linking them to cancer risk have not been fully clarified so far. This study explored LINC00578 rs7430456's association with breast cancer susceptibility and LINC00578's role/mechanism in triple-negative breast cancer (TNBC).</p><p><strong>Methods: </strong>A total of 480 breast cancer patients and 460 controls were enrolled. LINC00578 rs7430456 genotyping and LINC00578 expression detection via RT-qPCR were performed. Functional assays (proliferation, migration, invasion) were conducted in TNBC cell lines, and the LINC00578-miR-143-5p interaction was explored by dual-luciferase reporter assay.</p><p><strong>Results: </strong>LINC00578 rs7430456 G allele and AG/GG genotypes reduced breast cancer risk. LINC00578 was upregulated in breast cancer (especially TNBC) with an AUC of 0.873 for diagnosis. LINC00578 knockdown inhibited TNBC cell proliferation, migration, and invasion. LINC00578 sponged miR-143-5p, and miR-143-5p mediated its oncogenic effects.</p><p><strong>Conclusions: </strong>LINC00578 rs7430456 is associated with breast cancer susceptibility, and LINC00578 promotes TNBC progression via sponging miR-143-5p, being a potential biomarker and therapeutic target for breast cancer, particularly TNBC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13523219/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148470300","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}