HEREDITAS遗传
HEREDITAS,ISSN 0018-0661,中文译名:遗传 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
HEREDITAS 最新收录文献
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1. Haplotype-based validation of genomic regions for breeding of new Nordic apples.
PMID:日期:2026-08-12When 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.
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2. The prognostic value of miR-363-5p in colorectal cancer and its associated molecular mechanisms.
PMID:日期:2026-08-03Colorectal 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. 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. 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. 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.
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3. MicroRNA-345-3p expression inhibits colorectal cancer liver metastasis by targeting KHDRBS1 and TGF-β signaling pathway.
PMID:日期:2026-07-30The 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. 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. 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. 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.
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4. Targeting RASL12 by miR-6791-5p fuels malignant progression in lung adenocarcinoma.
PMID:日期:2026-07-25Lung 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. 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). 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. 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.
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5. miR-335-3p acts as a tumor suppressor in esophageal squamous cell carcinoma and predicts favorable prognosis.
5. miR-335-3p作为食管鳞状细胞癌的肿瘤抑制因子并预示良好预后PMID:日期:2026-07-21Esophageal 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. Verifying the involvement of miR-335-3p in the pathogenesis of esophageal squamous cell carcinoma (ESCC). 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. 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. 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.
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6. SNP rs7430456 mediated LINC00578 drives triple negative breast cancer through regulating miR-143-5p expression.
PMID:日期:2026-07-17A 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). 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. 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. 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.
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7. BFLF1 gene polymorphisms are associated with increased mortality in patients with EBV-associated diseases.
PMID:日期:2026-07-14Epstein-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. 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. 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)]. 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.
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8. miR-1-3p, as a novel diagnostic and prognostic biomarker, aggravates pancreatic acinar cell injury in acute pancreatitis by targeting GNPTAB.
PMID:日期:2026-07-10The 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. 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. 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. 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.
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9. {"_":"Identification of FOXK1 and SEMA7A as key genes associated with mA-related programmed cell death in diabetic retinopathy.","sup":["6"]}
9. {“_”：“确定FOXK1和SEMA7A是与糖尿病视网膜病变中mA相关程序性细胞死亡相关的关键基因。”，“sup”：[“6”]}PMID:日期:2026-07-10[中文摘要] 糖尿病视网膜病变（DR）是糖尿病一种严重的微血管并发症，其发病机制复杂，与程序性细胞死亡（PCD）以及N6-甲基腺苷（m⁶A）修饰密切相关。本研究旨在利用转录组数据筛选DR中与m⁶A相关PCD的关键基因，为DR的发病机制提供新靶点和理论依据。本研究从公共数据库获取DR样本和对照样本的转录组数据，同时从文献中检索m⁶A和PCD相关基因。通过差异表达分析和相关性分析鉴定候选基因。利用构建的蛋白质-蛋白质相互作用（PPI）网络，采用机器学习算法筛选特征基因，并对这些基因进行表达验证以确定关键基因。随后构建预测列线图并评估其性能。进行富集分析和免疫浸润分析。最后，构建分子调控网络并进行分子对接。初步鉴定出DR与对照样本之间的3，716个差异表达基因（DRDEGs）。通过将DRDEGs与PCD相关基因及m⁶A相关差异表达基因取交集，并进行Spearman相关性分析，鉴定出58个候选基因。随后，通过PPI、机器学习和表达分析，确定叉头框K1（FOXK1）和Semaphorin 7A（SEMA7A）为关键基因。此外，这两个关键基因构建了一个准确性良好的DR诊断列线图。GSEA揭示了它们在DR发病机制中的关键作用。此外，免疫浸润分析突出了免疫失调在DR中的参与。构建的TF-mRNA-miRNA调控网络包含2个关键基因、14个转录因子和12个miRNA（如BRCA1-FOXK1-mmu-miR-7234-3p）。分子对接显示地西他滨等药物与FOXK1结合良好，值得进一步实验研究其治疗效果。本研究确定了FOXK1和SEMA7A是与m⁶A相关程序性细胞死亡相关的DR关键基因，可能为后续诊断和治疗研究提供新方向。
[英文摘要] 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 (mA) modification. The objective of this research was to pinpoint crucial genes related to mA-related PCD in DR using transcriptomic data, offering novel targets and a theoretical basis for the pathogenesis of DR. In this study, transcriptomic data of DR samples and control samples were obtained from a public database. Meanwhile, mA-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. 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. This study identified FOXK1 and SEMA7A as key genes in DR related to mA-associated programmed cell death, which may provide a new direction for subsequent research on diagnosis and treatment.
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10. 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.
PMID:日期:2026-07-09MiR-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. 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. 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. 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.