Hereditas最新文献

{"title":"In silico and in vitro assessment of TP53, ATM, RAD51, and BAX genes in gastric cancer and their contribution to radiotherapy resistance.","authors":"Junwei Zhang, Pengtao He","doi":"10.1186/s41065-025-00496-3","DOIUrl":"10.1186/s41065-025-00496-3","url":null,"abstract":"<p><strong>Background: </strong>Gastric cancer remains a leading cause of cancer-related morbidity and mortality worldwide. The genetic factors contributing to gastric cancer progression and resistance to therapies, particularly radiotherapy, are not fully understood. TP53, ATM, RAD51, and BAX are genes involved in DNA repair, apoptosis, and response to stress. The aim of this study was to investigate the expression patterns of these genes in gastric cancer, their potential role in radiotherapy resistance, and their diagnostic value.</p><p><strong>Methodology: </strong>Gene expression levels of TP53, ATM, RAD51, and BAX were assessed using RT-qPCR across 9 gastric cancer cell lines and 6 normal control cell lines. Additionally, protein expression was confirmed via IHC and TCGA dataset analysis. Methylation levels of these genes were evaluated in gastric cancer tissues using the GSCA database. Mutational analysis was conducted using cBioPortal, and survival analysis was performed using Kaplan-Meier and meta-analysis. The radiotherapy resistance study was carried out by knocking down TP53, RAD51, and BAX in AGS and MKN-45 gastric cancer cell lines, followed by expression analysis, colony formation, and wound healing assays.</p><p><strong>Results: </strong>The expression of TP53, RAD51, and BAX was significantly upregulated, while ATM was downregulated in gastric cancer cell lines compared to normal controls. All four genes demonstrated good discriminatory power (AUC = 1) in distinguishing gastric cancer from normal samples. Methylation analysis revealed significant hypomethylation of TP53, RAD51, and BAX, and hypermethylation of ATM in gastric cancer tissues. Mutational analysis showed that TP53 was altered in 88% of gastric cancer samples, while ATM, RAD51, and BAX exhibited lower mutation rates. Survival analysis suggested that elevated expression of TP53, RAD51, and BAX may be linked to poorer survival outcomes, while reduced ATM expression appeared to associate with decreased overall survival. However, these associations require further validation through additional studies. Knockdown of TP53, RAD51, and BAX in AGS and MKN-45 cells resulted in significantly reduced cell proliferation and slower wound healing, highlighting their role in radiotherapy resistance.</p><p><strong>Conclusion: </strong>The TP53, RAD51, and BAX genes are significantly involved in gastric cancer progression and resistance to radiotherapy. Their expression and mutation status provide valuable diagnostic and prognostic information.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"125"},"PeriodicalIF":2.7,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255106/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144617148","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":"LncRNA SDCBP2-AS1 is a putative biomarker for postmenopausal osteoporosis and promotes osteogenic differentiation of BMSCs by regulating miR-361-3p.","authors":"Jindong Chen, Shilong Zhang, Dixin Cai, Qing Yin, Qian Xie, Pengfang Xu, Junling Zhu","doi":"10.1186/s41065-025-00494-5","DOIUrl":"10.1186/s41065-025-00494-5","url":null,"abstract":"<p><strong>Background: </strong>Numerous long noncoding RNAs (lncRNAs) have been proven to participate in osteogenesis and postmenopausal osteoporosis (PMOP). We measured serum SDCBP2-AS1 expression changes in patients with PMOP and investigated its effects on osteoblast differentiation in human bone marrow-derived mesenchymal stem cells (hBMSC) cells.</p><p><strong>Methods: </strong>RT-qPCR was used to measure SDCBP2-AS1 levels and the expression of osteogenic differentiation indicators. The diagnostic efficacy of SDCBP2-AS1 was assessed using a receiver operating characteristic (ROC) analysis. CCK-8 and flow cytometry methods were employed to investigate the functional impact of SDCBP2-AS1 on hBMSC cell proliferation and apoptosis during osteoblast differentiation. The bioinformatics, dual-luciferase reporter assay, and RNA Immunoprecipitation (RIP) assay were used to identify and confirm SDCBP2-AS1/miR-361-3p interaction.</p><p><strong>Results: </strong>Serum SDCBP2-AS1 was decreased in patients with PMOP, especially in those with fractures. The SDCBP2-AS1 levels were positively correlated with patients' T scores and BMDs. Decreased SDCBP2-AS1 had a certain high area under the ROC curve (AUC) value (AUC = 0.81) in distinguishing PMOP patients with fractures from those without fractures. SDCBP2-AS1 levels gradually increased after four weeks of treatment in PMOP patients and hBMSCs during cell differentiation. Enhanced SDCBP2-AS1 promoted cell proliferation and the levels of osteoblast differentiation markers, including ALP, OCN, RUNX2, and Collagen I, while decreasing cell apoptosis. miR-361-3p was a direct target of SDCBP2-AS1. The influence of SDCBP2-AS1 on cell activities and hBMSCs differentiation was diminished by miR-361-3p.</p><p><strong>Conclusions: </strong>SDCBP2-AS1 might be a diagnostic biomarker in predicting PMOP patients with fractures. By measuring the levels of SDCBP2-AS1 in patient samples, clinicians may be able to identify those who are more susceptible to bone fractures, enabling earlier and more targeted preventive measures. SDCBP2-AS1 targeting miR-361-3p regulates the osteogenic differentiation of hBMSCs, which might be a new target for the treatment of PMOP.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"124"},"PeriodicalIF":2.7,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608173","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":"METTL3 mediates m6A methylation modification of ULBP2 and affects the progression of cervical cancer.","authors":"Hongtao Ren, Yuting Wang, Jiao Yu, Lei An, Xiulong Ma, Jiyuan Pan","doi":"10.1186/s41065-025-00483-8","DOIUrl":"10.1186/s41065-025-00483-8","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer (CC) is one of the most prevalent malignancies in women, posing a significant challenge globally. However, the precise molecular mechanism regulating CC progression through methyltransferase-like protein 3 (METTL3) and UL16 Binding Protein 2 (ULBP2) remains largely unknown.</p><p><strong>Methods: </strong>Bioinformatic analysis was used to identify the effect of ULBP2 expression in CC tissues. RT-qPCR and western blotting were employed to assess the mRNA and protein expression in CC cells and tissues. Methylthiazolyldiphenyl-tetrazolium bromide (MTT), 5‑Ethynyl‑2'‑deoxyuridine (EdU), wound healing, and transwell assays were utilized to estimate cell viability, proliferation, and metastasis, respectively. Cell apoptosis was detected by flow cytometry. CC cells were treated with different doses of radiotherapy. The m6A level was measured using methylated RNA immunoprecipitation (MeRIP) assay. A xenograft assay was conducted to further verify the roles of ULBP2 in CC.</p><p><strong>Results: </strong>ULBP2 was upregulated in CC. Downregulation of ULBP2 restrained the proliferation, metastasis and radiotherapy resistance of CC cells. METTL3 regulated m6A methylation modification of ULBP2. Insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1) promoted m6A methylation modification of ULBP2. METTL3 influenced the expression of ULBP2 and impacted the biological function of the CC cells. Silencing ULBP2 reduced the radioresistance of CC in vivo. Radiotherapy altered the gut microbiota in CC patients.</p><p><strong>Conclusion: </strong>METTL3 modulated the m6A methylation of ULBP2, affecting the oncogenic properties and radioresistance of CC cells.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"123"},"PeriodicalIF":2.7,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12243326/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144608174","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":"Translocations associated with colour-sidedness are common in northern Swedish cattle breeds.","authors":"Julia Hinken, Tytti Vanhala, Marta Gòdia, Martin Johnsson, Anna M Johansson","doi":"10.1186/s41065-025-00481-w","DOIUrl":"10.1186/s41065-025-00481-w","url":null,"abstract":"<p><p>The Swedish Mountain cattle and four other native Swedish cattle breeds show the phenotype of colour-sidedness. The causes of this phenotype are either a translocation and duplication from chromosome 6 to chromosome 29 (known as Cs₂₉) including the KIT gene, or an additional translocation allele where part of Cs₂₉ has been translocated back to chromosome 6 (Cs₆). Besides the colour-sidedness, the Cs₂₉ translocation has been associated with gonadal hypoplasia which can cause fertility problems. Despite breeding efforts during more than 80 years to reduce the prevalence of gonadal hypoplasia, there are still individuals with gonadal hypoplasia. We genotyped the Cs₂₉ and Cs₆ alleles in Swedish Mountain cattle and five other Swedish native breeds. Whole-genome sequence data of 30 cattle were analysed for the translocations, and 115 DNA samples were analysed using multiplex PCR. The current allele frequency of the Cs₂₉ allele in Swedish mountain cattle was estimated to be 44%. The results indicate that the Cs₂₉ translocation is also present in the four other native Swedish cattle breeds with colour-sidedness, and the Cs₆ translocation in at least three of them.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"122"},"PeriodicalIF":2.7,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583759","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":"WMRCA + : a weighted majority rule-based clustering method for cancer subtype prediction using metabolic gene sets.","authors":"Guojun Liu, Zhaopo Zhu, Yongqiang Xing, Hu Meng, Khyber Shinwari, Ningkun Xiao, Guoqing Liu","doi":"10.1186/s41065-025-00487-4","DOIUrl":"10.1186/s41065-025-00487-4","url":null,"abstract":"<p><p>Accurate classification of cancer subtypes plays a pivotal role in advancing precision medicine. In this study, we introduce WMRCA + , a novel clustering approach based on a weighted majority rule that integrates multi-omics data and incorporates metabolic gene sets to robustly determine the optimal number of clusters for tumor subtype identification. WMRCA + evaluates clustering performance using ten internal metrics and offers comprehensive functionalities for data preprocessing and visualization. When applied to The Cancer Genome Atlas (TCGA) lung cancer dataset using lipid metabolism-related gene sets, WMRCA + outperformed widely used clustering algorithms-including iCluster, SNF, NMF, CC, and CNMF-achieving an AUC of 0.947. WMRCA + provides robust, interpretable, and biologically meaningful clustering results, offering a valuable tool for improving the accuracy of cancer subtype prediction. The WMRCA + R package is freely available at https://github.com/guojunliu7/WMRCA .</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"121"},"PeriodicalIF":2.7,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583760","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 components in scorpion and centipede traditional Chinese medicine formulations with potentially beneficial actions in asthma: network pharmacology and molecular docking.","authors":"Yi-Ren Chen, Ya-Da Zhang, Wei Zhang, Bin-Qing Tang","doi":"10.1186/s41065-025-00490-9","DOIUrl":"10.1186/s41065-025-00490-9","url":null,"abstract":"<p><strong>Background: </strong>The aim of this study is to identify the principal active components of scorpion and centipede-derived traditional Chinese medicine (TCM) ingredients using network pharmacology and explore their mechanisms of action in the treatment of asthma.</p><p><strong>Methods: </strong>The chemical constituents and target information pertaining to scorpion and centipede-derived TCM components were obtained from the Traditional Chinese Medicine System Pharmacology (TCMSP) database and an herbal database. Asthma-related target genes were retrieved from the GeneCards and the Online Mendelian Inheritance in Man (OMIM) databases. The \"component-target\" network was constructed with the identified target genes using \"Cytoscape 3.9.2\" software, and the protein-protein interaction (PPI) network was generated in conjunction with the String database to further identify the core targets. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and gene ontology (GO) functional enrichment analysis were carried out on the targets associated with scorpion and centipede-derived TCM components. Molecular docking was subsequently performed using Autodock Vina software to validate the results. Asthma mouse model was established, and mouse lung tissues were collected for histopathological examination. The levels of TP53, HSP90AA1, and IL-17 mRNA in the mouse lung tissues were evaluated.</p><p><strong>Results: </strong>A total of 11 active components met the screening conditions, including 4 centipede-derived components and 7 scorpion-derived components. The key components identified included histamine, L-histidine, stearin, cholesteryl ferulate, and cholesterol, among others. Targets with degree values ≥ 16 included TP53, HSP90AA1, HSP90AB1, steroid receptor coactivator (SRC), epidermal growth factor receptor (EGFR), estrogen receptor 1 (ESR1), mitogen-activated protein kinase 1 (MAPK1), mitogen-activated protein kinase 3 (MAPK3), and histone deacetylase 1 (HDAC1). The pathways involved comprised calcium signaling, estrogen signaling, arachidonic acid metabolism, inflammatory mediator and transient receptor potential (TRP) signaling, vascular smooth muscle contraction, thyroid hormone signaling, sphingolipid signaling, IL-17 signaling, insulin resistance, and human cytomegalovirus infection pathways. Furthermore, the mouse experiments showed that SC improved inflammatory cell infiltration and mucus secretion in mouse lung tissues and significantly suppressed the expression of TP53, HSP90AA1, and IL-17 mRNA (all p < 0.05).</p><p><strong>Conclusion: </strong>Scorpion and centipede-derived active components may exert therapeutic effects in asthma treatment through potential targets such as TP53, HSP90AA1, HSP90AB1, SRC, EGFR, ESR1, MAPK1, MAPK3, and HDAC1.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"120"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12217821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553344","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":"TIMP1 promotes microglia M2 polarization through MAPK pathway to ameliorate early brain injury after ischemia.","authors":"Kangkang Zhao, Zizhao Huang","doi":"10.1186/s41065-025-00491-8","DOIUrl":"10.1186/s41065-025-00491-8","url":null,"abstract":"<p><strong>Objective: </strong>To explore the molecular regulatory mechanisms and biomarkers in regulating early brain injury (EBI) and inflammatory response after ischemic stroke (IS).</p><p><strong>Methods: </strong>Gene expression profiles of GSE148350, GSE35338, and GSE58294 were analyzed to screen the core genes involved in EBI after IS. Middle cerebral artery occlusion and reperfusion (MCAO/R) model and oxygen and glucose deprivation and reoxygenation (OGD/R) model were used to construct in vivo and in vitro IS models. In MCAO/R model, the effects of tissue inhibitor of metalloproteinase-1 (TIMP1) were investigated by Zea longa score, brain water content assessment and histological analysis. In OGD/R model, after TIMP1 was overexpressed in BV2 cells, M1 and M2 polarization markers (iNOS and Arg-1) in BV2 cells were detected by Western blot, and the effects of BV2 on the viability and apoptosis of HT22 cells were evaluated by cell counting kit-8 and flow cytometry, respectively. Additionally, the effects of TIMP1 overexpression on MAPK pathway in BV2 cells were also detected by Western blot.</p><p><strong>Results: </strong>Two core genes, TIMP1 and vimentin (VIM) were screened from 254 differentially expressed genes in IS. TIMP1 was closely associated with the dysregulation of immune cell infiltration. TIMP1 overexpression significantly mitigated MCAO/R-induced neurological dysfunction, brain edema, neuronal apoptosis and inflammatory response in rats. In vitro, it was revealed that TIMP1 overexpression in BV2 cells increased viability and inhibited apoptosis of HT22 cells. In BV2 cells, TIMP1 overexpression promoted the expression of Agr-1 and inhibited the expression of iNOS. In addition, overexpression of TIMP1 inhibited OGD/R-induced increases in the phosphorylation levels of p38, JNK and ERK proteins in BV2 cells.</p><p><strong>Conclusion: </strong>This study identified a post-IS EBI regulator, TIMP1. TIMP1 promotes M2 polarization of microglia and ameliorate neurological injury after IS by inactivating MAPK signaling pathway.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"119"},"PeriodicalIF":2.7,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12217830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553355","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":"Global research trends in the relationship between diabetic cardiomyopathy and mitochondria: a bibliometric analysis.","authors":"Jiajie Li, Jinxing Liu, Yaping Wang, Heguo Yan, Qin Li, Weibo Wen","doi":"10.1186/s41065-025-00488-3","DOIUrl":"10.1186/s41065-025-00488-3","url":null,"abstract":"<p><strong>Background: </strong>Diabetic Cardiomyopathy (DCM) is a distinct form of heart disease whose pathogenesis remains largely elusive. Recent studies have shed light on the significant role of mitochondria in the development of DCM, emphasizing their critical involvement. Despite these advancements, a bibliometric analysis focusing on the nexus between mitochondria and DCM has not been conducted, leaving a gap in a holistic understanding of research trends in this field.</p><p><strong>Methods: </strong>This study extracted publications addressing the role of mitochondria in DCM from the Web of Science Core Collection, spanning from 1988 to 2024. A detailed bibliometric analysis was undertaken using tools like CiteSpace, VOSviewer, Microsoft Excel, and Tableau Public to assess the data.</p><p><strong>Results: </strong>The analysis encompassed 440 publications involving 2705 researchers from 1457 institutions across 175 countries/regions. These studies were disseminated across 202 journals. China was the most prolific country with 192 publications, followed by the United States with 156, and Canada with 26. E. Dale Abel emerged as the most prolific author in this area. Key journals contributing to this research included the American Journal of Physiology-Heart and Circulatory Physiology and the Journal of Molecular and Cellular Cardiology. The future research direction is likely to focus deeper into the mechanisms of mitochondrial dysfunction in the diabetic heart and to identify molecular and cellular targets for therapeutic intervention.</p><p><strong>Conclusion: </strong>This report presents the first detailed bibliometric review of the intersection between mitochondrial research and DCM. It offers critical insights and guidance for researchers aiming to navigate and contribute to this evolving area of study.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"114"},"PeriodicalIF":2.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12210778/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540031","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":"Trends and hotspots in autoimmune hepatitis research: based on bibliometric analysis.","authors":"Ruisi Li, Yue Xu, XiaoYing Xu, YiHeng Xu, Haitang Huang, Xiaojuan Lv, Chu Liao, Junqiu Ye, Bo Liu, Hengfei Li","doi":"10.1186/s41065-025-00477-6","DOIUrl":"10.1186/s41065-025-00477-6","url":null,"abstract":"<p><strong>Background: </strong>Autoimmune Hepatitis (AIH) is a chronic inflammatory liver disease characterized by a sustained inflammatory response in the liver, usually associated with abnormalities in the immune system.The purpose of this study was to utilize bibliometric analysis to assess the current state of research on AIH and to predict future research areas and emerging trends.</p><p><strong>Objective: </strong>In this study, we used bibliometric analysis to comprehensively analyze the literature on Autoimmune Hepatitis (AIH) published during the past two decades.</p><p><strong>Methods: </strong>Literature from 2003 to 2023 was retrieved from the Web of Science Core Collection, the world's leading citation indexing database. Visualization and analysis were performed using VOSviewer 1.6.18 and CiteSpace 6.2.R3 software.</p><p><strong>Results: </strong>The study covered 6,390 papers by 28,037 authors from 291 institutions in 110 countries. AIH research output grew significantly, peaking in 2023. The US was the top contributor, followed by China and Japan. Notable institutions included the University of London, Mayo Clinic, and King's College Hospital NHS Foundation Trust. AIH research spans medicine, healthcare, clinical sciences, molecular biology, immunology, etc. CONCLUSION: In this paper, we have used bibliometric analysis to systematically review and analyze the research literature on autoimmune hepatitis (AIH) over the past two decades. This comprehensive overview aims to provide scholars dedicated to this field with a clear research lineage and future research directions.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"115"},"PeriodicalIF":2.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12211198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540033","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":"Clinical significance and biological function of PRKCQ-AS1/miR-582-3p expression in LUAD.","authors":"Lingling Liu, Xiaofen Liu, Xiaojiao Wu, Hang Fang, Jingjing Shi, Wei Jiang","doi":"10.1186/s41065-025-00482-9","DOIUrl":"10.1186/s41065-025-00482-9","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the clinical value and mechanism of action of long non-coding RNA PRKCQ-AS1 for lung adenocarcinoma (LUAD) progression.</p><p><strong>Methods: </strong>Clinical data of 128 LUAD patients were collected, postoperative pathological tissues were stored at -80 °C. Kaplan-Meier survival analysis was employed to investigate differences in 5-year survival rates across various expression groups, while Cox regression models assessed the prognostic factors influencing patient outcomes. Reverse transcription quantitative PCR (RT-qPCR) was utilized to measure the expression levels of PRKCQ-AS1 and miR-582-3p in pathological tissues and LUAD cell lines. Additionally, a dual-luciferase reporter assay validated the reciprocal relationship. CCK8 examined cell proliferation, Transwell observed cell migration and invasion.</p><p><strong>Results: </strong>PRKCQ-AS1 was down-regulated and miR-582-3p was up-regulated in LUAD tissues and cell. PRKCQ-AS1 and miR-582-3p expression affects some pathological features (lymph node metastasis, TNM stage, tumour differentiation) in LUAD patients. Patients with low PRKCQ-AS1 and high miR-582-3p had increased mortality. Interaction of PRKCQ-AS1 targeting miR-582-3p exists in LUAD cells. RGMB, STXBP6 are downstream target genes of miR-582-3p. Overexpression of (oe-) PRKCQ-AS1 inhibited LUAD cell proliferation, migration, and invasion. However, concomitant use of miR-582-3p mimics resisted the effects of PRKCQ-AS1 overexpression on cells.</p><p><strong>Conclusion: </strong>PRKCQ-AS1/miR-582-3p axis regulatory relationship exists in lung adenocarcinoma cells. PRKCQ-AS1 may regulate the proliferation, migration and invasion of lung adenocarcinoma cells and participate in LUAD regulation by targeting miR-582-3p.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"116"},"PeriodicalIF":2.7,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12211715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540018","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}