Hereditas最新文献

{"title":"BFLF1 gene polymorphisms are associated with increased mortality in patients with EBV-associated diseases.","authors":"Xurong Li, Jing Wu, Shenglei Yu, Zhe Zhou, Wenhong Zhang, Lingyun Shao, Ning Jiang, Qingluan Yang","doi":"10.1186/s41065-026-00708-4","DOIUrl":"10.1186/s41065-026-00708-4","url":null,"abstract":"<p><strong>Objective: </strong>Epstein-Barr virus (EBV) -associated diseases comprise a spectrum of conditions, including infectious mononucleosis (IM) and chronic active EBV infections (CAEBV), as well as malignant lymphomas. The study aimed to compare genomic variations of Type 1 EBV across different subtypes of EBV-associated diseases to investigate the impact of EBV variants on disease progression and clinical outcomes.</p><p><strong>Methods: </strong>A total of 36 patients with EBV-associated diseases were enrolled. Targeted EBV genome sequencing on EBV genomic was performed with peripheral blood DNA samples (400µL) using Illumina sequencing technology. Following quality control with FastQC, Fastp, and TriTrimmomatic, 27 samples comprising 2 IM, 9 CAEBV and 16 NK/T-cell lymphoma cases meeting the critera of minimum effective coverage > 10 and coverage > 80% were retained. Single nucleotide polymorphisms (SNP) annotations were generated into VCF files, and variant profiles were visualized using heatmaps. Variant rates were compared using Fisher's exact test, based on disease subtype, presence of hemophagocytic lymphohistiocystosis (HLH), and clinical outcomes. Odds ratios (ORs) were calculated using the Haldane-Anscombe correction.</p><p><strong>Results: </strong>Compared with the reference stain B95.8/Raji, a total of 2182 variants were identified in 27 samples. The variants located in coding region included 523 missense variants, 1 insertion, and 2 deletion, all of which only involved single amino acid changes in the encoded proteins. Although a large number of variants were detected, no statistically significant differences were observed among the IM, CAEBV and lymphoma groups, or between patients with and without HLH. However, three variants in BFLF1 were significantly more frequent in deceased patients compared to survivors, which detailedly refers to Ile35Thr, Asp44Glu and Val246Ile [P = 0.0267, OR = 15.00, 95%CI= (0.7436,301.5)].</p><p><strong>Conclusion: </strong>Single amino acid changes in EBV proteins had no significant effect on the progression status of EBV-associated diseases, but the variants in BFLF1 were associated with an increased risk of mortality.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148445914","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-1-3p, as a novel diagnostic and prognostic biomarker, aggravates pancreatic acinar cell injury in acute pancreatitis by targeting GNPTAB.","authors":"Haibin Huang, Jinyu Liu, Lianjun Wu, Wen Miao","doi":"10.1186/s41065-026-00704-8","DOIUrl":"10.1186/s41065-026-00704-8","url":null,"abstract":"<p><strong>Objective: </strong>The mechanisms underlying the progression of acute pancreatitis (AP) remain incompletely elucidated. This study investigates the expression pattern, diagnostic and prognostic value of miR-1-3p in AP patients, and further elucidates its role in pancreatic acinar cell injury and the underlying molecular mechanisms.</p><p><strong>Methods: </strong>miR-1-3p levels were measured via qPCR and correlated with clinical indicators. ROC analysis evaluated diagnostic efficacy, and logistic regression assessed prognostic relevance. A Caerulein-induced injury model was established in MPC-83 cells. Post-transfection with a miR-1-3p inhibitor, cell viability (CCK-8), inflammatory factors (ELISA), and oxidative stress (WST-8/TBA) were evaluated. Bioinformatics-predicted target genes were validated through dual-luciferase reporter and RIP assays, with rescue experiments confirming the targeting relationship.</p><p><strong>Results: </strong>miR-1-3p was significantly upregulated in SAP patients and effectively distinguished healthy individuals (AUC = 0.880) and disease severity (AUC = 0.878). Its levels positively correlated with CRP, APACHE II, and BUN (p < 0.0001). High miR-1-3p expression independently predicted poor prognosis (OR = 9.54, p = 0.023). Inhibition of miR-1-3p alleviated Caerulein-induced cellular injury in vitro. GNPTAB was identified as a direct target, showing downregulation and negative correlation with miR-1-3p in patients. Rescue experiments confirmed that GNPTAB downregulation partially reversed the protective effects of miR-1-3p inhibition.</p><p><strong>Conclusions: </strong>miR-1-3p, upregulated in SAP, is a potential diagnostic biomarker and predictor of poor prognosis. It exacerbates pancreatic acinar cell injury by targeting GNPTAB, contributing to inflammation, oxidative stress, and AP progression.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13640367/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420636","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 FOXK1 and SEMA7A as key genes associated with m⁶A-related programmed cell death in diabetic retinopathy.","authors":"Jie Yang, Zhenyu Wu, Ningning Dong","doi":"10.1186/s41065-026-00710-w","DOIUrl":"10.1186/s41065-026-00710-w","url":null,"abstract":"<p><strong>Background: </strong>Diabetic retinopathy (DR), a serious microvascular complication of diabetes, has a complex pathogenic mechanism that is intricately linked to programmed cell death (PCD) and also to N6-methyladenosine (m⁶A) modification. The objective of this research was to pinpoint crucial genes related to m⁶A-related PCD in DR using transcriptomic data, offering novel targets and a theoretical basis for the pathogenesis of DR.</p><p><strong>Methods: </strong>In this study, transcriptomic data of DR samples and control samples were obtained from a public database. Meanwhile, m⁶A-and PCD-related genes were retrieved from the literature. Candidate genes were identified via differential expression and correlation analyses. Using constructed protein-protein interaction (PPI) networks, a machine learning algorithms screened for feature genes, which underwent expression validation to determine key genes. A predictive nomogram was subsequently developed and its performance evaluated. Enrichment analysis, along with immune infiltration analysis were carried out. Finally, molecular regulatory networks and molecular docking was performed.</p><p><strong>Results: </strong>Initially, 3,716 differentially expressed genes between DR and control samples (DRDEGs) were identified. By intersecting DRDEGs with PCD-related genes and m⁶A-related differentially expressed genes, followed by Spearman correlation analysis, 58 candidate genes were identified. Subsequently, Forkhead box K1 (FOXK1) and Semaphorin 7 A (SEMA7A) were identified as key genes through PPI, machine learning, and expression analyses. Furthermore, the two key genes constructed a well accurate nomogram for DR diagnosis. GSEA revealed their critical roles in DR pathogenesis. Moreover, immune infiltration analysis highlighted the involvement of immune dysregulation in DR. The constructed TF-mRNA-miRNA regulatory network contained 2 key genes, 14 transcription factors, and 12 miRNAs (e.g. BRCA1-FOXK1-mmu-miR-7234-3p). Molecular docking showed that decitabine and other drugs bound well to FOXK1,warranting further experimental investigation into their therapeutic efficacy.</p><p><strong>Conclusion: </strong>This study identified FOXK1 and SEMA7A as key genes in DR related to m⁶A-associated programmed cell death, which may provide a new direction for subsequent research on diagnosis and treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13640323/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420631","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-146b-5p serves as a novel biomarker for acute myocardial infarction and is involved in regulating oxidized low-density lipoprotein-induced endothelial injury through targeting PRKAR2A.","authors":"Hailiang Wu, Hui Zhang, Yuyan Hou, Zhifang Wang, Yang Bian","doi":"10.1186/s41065-026-00706-6","DOIUrl":"10.1186/s41065-026-00706-6","url":null,"abstract":"<p><strong>Background: </strong>MiR-146b-5p, a disease-responsive miRNA with circulatory stability, has been implicated in multiple pathologies, but its role in acute myocardial infarction (AMI) remains unexplored. The objective of this study was to explore the role of miR-146b-5p in AMI.</p><p><strong>Methods: </strong>Serum from 103 AMI patients and 95 healthy controls was analyzed via qRT-PCR to quantify miR-146b-5p/PRKAR2A expression, with ROC curves evaluating diagnostic performance and correlation analyses linking miR-146b-5p levels to clinical indicators of AMI severity. Prognostic associations were systematically assessed using Kaplan-Meier curves and COX regression models. In vitro ox-LDL-induced HCAEC injury models employed CCK-8 assays, flow cytometry, Caspase-3 activity measurements, ELISA, and oxidative stress assays to elucidate cellular mechanisms. Dual-luciferase reporter and Western blot assays assessed the relation between miR-146b-5p and PRKAR2A.</p><p><strong>Results: </strong>Upregulated miR-146b-5p expression was observed in AMI compared with the HC group, showing diagnostic value and correlation with hs-CRP, CK-MB, cTnI, LVEF, and Killip grade. Higher miR-146b-5p expression predicted poor prognosis of AMI. In ox-LDL-induced HCAECs, miR-146b-5p inhibition reduced apoptosis, inflammation (IL-1β, TNF-α), and endothelial dysfunction marker levels (ET-1, vWF), while promoting proliferation. PRKAR2A was downregulated in ox-LDL and confirmed as a miR-146b-5p target, with its knockdown reversing the protective effects of miR-146b-5p inhibition on ox-LDL-induced HCAEC injury.</p><p><strong>Conclusions: </strong>Upregulated miR-146b-5p, which correlated with AMI severity, demonstrated diagnostic and prognostic potential for AMI. It promoted AMI progression by aggravating endothelial injury under ox-LDL induction through suppressing PRKAR2A.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13584393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148420600","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":"Whole blood miRNA expression signatures as predictors of neoadjuvant chemotherapy response in triple-negative breast cancer.","authors":"Monika Drobniene, Domas Stitilis, Linas Kunigenas, Egle Strainiene, Sonata Jarmalaite, Kestutis Suziedelis","doi":"10.1186/s41065-026-00712-8","DOIUrl":"10.1186/s41065-026-00712-8","url":null,"abstract":"<p><strong>Background: </strong>Triple negative breast cancer (TNBC) is an aggressive malignancy distinguished by resistance to standard breast cancer therapies. The absence of reliable prognostic tools hinders the ability to predict therapeutic response, resulting in some patients receiving treatment that is ineffective yet physically exhausting. miRNAs are small non-coding RNA molecules that regulate gene expression, and their dysregulated profiles in liquid biopsies hold immense potential as minimally invasive biomarkers for monitoring treatment response.</p><p><strong>Results: </strong>In this study, we seek to identify miRNAs that may serve as predictive biomarkers for therapeutic responses in patients diagnosed with triple-negative breast cancer. To achieve this, an in silico analysis of the Cancer Genome Atlas (TCGA) dataset is conducted to narrow the list of candidate miRNAs. miRNAs with potential involvement in TNBC were selected for clinical validation in whole-blood samples of TNBC patients before and after therapy. The RT-qPCR-based expression analysis revealed significant predictive potential of miR-340-5p, miR-1307-3p, miR-185-5p, and miR-30a-3p.</p><p><strong>Conclusions: </strong>Our study identified that dysregulated miRNA signatures can serve as independent indicators for therapeutic monitoring. Notably, the combined multi-miRNA expression panel offers a robust, superior predictive value for stratifying treatment response and tracking disease progression in TNBC patients.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13632267/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148411515","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 and experimental validation of biomarkers associated with T cell infiltration in psoriasis.","authors":"Li Zhang, Xiao-Yan Yang, Fa-Zeng Li, Zhi-Quan Liu, Lei Zhang, Zheng-Fa Ou","doi":"10.1186/s41065-026-00707-5","DOIUrl":"10.1186/s41065-026-00707-5","url":null,"abstract":"<p><strong>Background: </strong>Psoriasis represents a prevalent long-term inflammatory skin condition marked by the dysregulation of immune responses. T cells are integral to the pathogenesis of psoriasis. This study conducted a comprehensive analysis to recognize biomarkers associated with T cell infiltration in psoriasis and to elucidate their underlying molecular mechanisms.</p><p><strong>Results: </strong>Three biomarkers (AKR1B10, C10orf99, and CKS2) demonstrated high sensitivity and specificity in receiver operating characteristic (ROC) curve, and the reliability of the developed nomogram diagnostic model was observed. In addition, gene set enrichment analysis (GSEA) revealed notable enrichment of the biomarkers in the NOD-like receptor signaling pathway and focal adhesion. Immune infiltration analysis indicated elevated levels of activated B cells and CD8 T cells in psoriasis samples, with the biomarkers showing meaningful correlations with the majority of immune cell infiltration statuses. Importantly, preliminary reverse transcription quantitative PCR (RT-qPCR) validation showed increased expression of AKR1B10, C10orf99, and CKS2 in psoriasis tissues, confirmed higher expression of AKR1B10, C10orf99, and CKS2 in psoriasis patients.</p><p><strong>Conclusion: </strong>AKR1B10, C10orf99, and CKS2 may serve as candidate molecules for future mechanistic studies and provide potential diagnostic biomarkers for further investigation of psoriasis-related immune regulation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13602608/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148382070","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":"M2 macrophage-derived exosomes promote the malignant progression and glycolysis of cervical cancer via Msi1.","authors":"Liting Sun, Abudureyimu Tunishahan, Xiaowen Li","doi":"10.1186/s41065-026-00703-9","DOIUrl":"10.1186/s41065-026-00703-9","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer is a common gynecologic malignancy characterized by high recurrence and metastasis rate. Exosomes derived from M2-polarized tumor-associated macrophages play a key role in promoting tumorigenesis and cancer progression. Additionally, musashi1 (Msi1) is a key oncoprotein across multiple malignancies. Therefore, this study aims to determine the role of M2 macrophage-derived exosomal Msi1 in cervical cancer progression and glycolysis and to clarify the underlying mechanism.</p><p><strong>Methods: </strong>M2 macrophages were identified using microscope, flow cytometry, and western blot. Gene mRNA and protein expression levels were analyzed via quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. The cell proliferation, invasion, apoptosis, and sphere formation were assessed using 5-Ethynyl-2'-deoxyuridine (EdU) staining, Transwell, flow cytometry, and sphere formation assay, respectively. The glucose uptake and lactate production were determined using commercial kits. Exosomes were identified using western blot, transmission electron microscopy, and nanoparticle tracking analysis (NTA). Cellular uptake of exosomes was assessed by incubating SiHa and Ca Ski cells with PKH67-labeled exosomes. Cervical cancer xenograft mouse models were established to analyze the role of M2 macrophage-derived exosomal Msi1.</p><p><strong>Results: </strong>Msi1 expression was increased in M2 macrophages (**P < 0.01 and ***P < 0.001). Functionally, M2 macrophages enhanced cervical cancer cell proliferation, invasion, aerobic glycolysis, and stemness as well as suppressed cell apoptosis through secreting exosomes (*P < 0.05, **P < 0.01, and ***P < 0.001). Importantly, Msi1 expression was increased in M2 macrophage-derived exosomes (***P < 0.001). Mechanically, M2 macrophage-derived exosomes promoted malignancy and glycolysis by carrying Msi1 (*P < 0.01 and ***P < 0.001). In vivo, M2 macrophage-derived exosomal Msi1 accelerated cervical cancer progression (***P < 0.001).</p><p><strong>Conclusion: </strong>M2 macrophage-derived exosomes promote cervical cancer progression and glycolysis by delivering Msi1 to recipient cells.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148328800","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":"KLF5 promotes proliferation, migration, and autophagy-/EMT‑associated molecular changes in lens epithelial cells via transcriptional activation of THBS1 in traumatic cataract.","authors":"Junjun Han, Tian Wang, Xin Yang, Xiaoli Li","doi":"10.1186/s41065-026-00701-x","DOIUrl":"10.1186/s41065-026-00701-x","url":null,"abstract":"<p><strong>Purpose: </strong>Traumatic cataract is a common blinding eye disease after ocular trauma, and its pathogenesis is closely related to lens epithelial cell dysfunction, while the definite molecular regulatory mechanism between upstream transcription factor and downstream target gene remains poorly clarified. This study aimed to clarify the role and molecular mechanism of the krüppel-like factor 5 (KLF5)/ thrombosponin 1 (THBS1) axis in regulating proliferation, migration, epithelial-mesenchymal transition and autophagy of lens epithelial cells in traumatic cataract, and to explore its potential clinical therapeutic value.</p><p><strong>Methods: </strong>The GSE295383 dataset in the gene expression omnibus (GEO) database was downloaded, and the differentially expressed genes (DEGs) were screened by linear models for microarray data (limma) package of R language. Combined with Weighted gene co-expression network analysis (WGCNA), the gene co-expression network was constructed and the key modules were screened. Gene ontology (GO), kyoto encyclopedia of genes and genomes (KEGG) and gene set enrichment analysis (GSEA) combined with human transcription factor target (hTFtarget) and JASPAR databases were used to predict the upstream transcription factors of THBS1. Subsequently, SRA01/04 cells were induced with transforming growth factor-beta 2 (TGF-β2) to construct a cataract cell model.</p><p><strong>Results: </strong>THBS1 and KLF5 were highly expressed in LECs exposed to TGF-β2. KLF5 could activate THBS1 transcription by binding to THBS1 promoter - 174 to -165 sites. Knockdown of THBS1 inhibited TGF-β2-induced viability, proliferation, migration, and altered the expression of epithelial-mesenchymal transition (EMT)- and autophagy-related markers in LECs. Knockdown of KLF5 downregulated THBS1 expression and produced a similar inhibitory effect, while overexpression of THBS1 reversed the effect of KLF5 knockdown.</p><p><strong>Conclusions: </strong>This study demonstrated that KLF5 promoted the proliferation, migration, and EMT‑associated molecular changes of LECs in traumatic cataract through transcriptional activation of THBS1, and regulated the expression of autophagy‑related markers in LECs, suggesting that KLF5/THBS1 axis might be a potential target for the treatment of traumatic cataract.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13555852/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148316999","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":"Development and validation of palmitoylation-related genes characteristics for prediction of prognosis and immune landscape in endometrial cancer.","authors":"Chuchu Zhao, Guiying Zhang","doi":"10.1186/s41065-026-00699-2","DOIUrl":"10.1186/s41065-026-00699-2","url":null,"abstract":"<p><strong>Background: </strong>Endometrial cancer (EC) is the most common cancer of the female reproductive system. Palmitoylation dysregulation is linked to various diseases. However, there is still insufficient research on its use as a prognostic marker for EC.</p><p><strong>Methods: </strong>This research utilized transcriptomic data and clinical characteristics from EC patients sourced from the TCGA database. Key palmitoylation-related genes (PRGs) were identified through a series of bioinformatics analyses, followed by the construction of a prognostic model. The mRNA expression levels of characteristic genes in EC cells and clinical samples were investigated through reverse transcription quantitative polymerase chain reaction (RT-qPCR). Immune infiltration analysis was performed using ssGSEA and CIBERSORT. The molecular subtypes of EC were identified by consensus clustering.</p><p><strong>Results: </strong>This study identified six PRGs, and the results of bioinformatic analysis of their mRNA expression patterns were consistent with experimental validation. A risk stratification model constructed based on these six PRGs was able to significantly distinguish between high-risk and low-risk patients in terms of survival prognosis, with patients in the low-risk group having a better prognosis than those in the high-risk group. Furthermore, immune characteristic heterogeneity was observed among different risk subgroups. Through consensus clustering analysis, EC samples were classified into two molecular subtypes with significant differences.</p><p><strong>Conclusion: </strong>This study constructed and validated a prognostic risk model for EC based on PRGs, which demonstrated potential for stratifying patient survival rates and characterizing immune microenvironment features in a retrospective dataset.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13540888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301305","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 role of miR-557 in modulating cervical cancer malignancy by targeting TAOK1.","authors":"Yilin Yin, Yingying Huang, Li Lin, Mingxiu Cui, Linge Zhong","doi":"10.1186/s41065-026-00695-6","DOIUrl":"10.1186/s41065-026-00695-6","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer (CC) remains a major threat to women's health globally. Although miR-557 is a tumor suppressor in multiple cancers, its role in CC remains unclear.</p><p><strong>Objective: </strong>This study investigated whether miR-557 regulates CC progression by targeting TAOK1.</p><p><strong>Methods: </strong>This study collected 113 pairs of cervical cancer tissues and adjacent tissues. The expression of miR-557 was detected by qRT-PCR, and its relationship with clinicopathological features and prognosis was analyzed. In HeLa and SiHa cell lines, we performed functional assays (CCK-8, Transwell) and measured ferroptosis-related indicators (Fe²⁺, GSH, GSH-Px) after transfecting miR-557 mimic or TAOK1 overexpression vectors. The miR-557/TAOK1 targeting relationship was validated by dual-luciferase reporter assay and rescue experiments.</p><p><strong>Results: </strong>miR-557 was significantly downregulated in CC tissues and cell lines. Low miR-557 expression correlated with advanced FIGO stage, LNM, and poor prognosis. Functionally, miR-557 overexpression inhibited CC cell proliferation, migration, and invasion, accompanied by increased Fe²⁺ levels and decreased GSH and GSH-Px activity. TAOK1 was identified as a direct target of miR-557, and its overexpression reversed the tumor-suppressive effects and ferroptosis-related changes induced by miR-557.</p><p><strong>Conclusions: </strong>miR-557 is significantly downregulated in CC and exerts tumor-suppressive functions. By targeting TAOK1, it inhibits the malignant progression of CC cells and may act as a promising biomarker for CC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13491869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148239264","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}