Hereditas最新文献

{"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":"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}

{"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":"https://doi.org/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":"","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":"","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":"https://doi.org/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":"","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":"","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":"https://doi.org/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":"","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":"","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":"https://doi.org/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":"","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":"","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":"https://doi.org/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":"","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":"","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":"https://doi.org/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":"","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":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}