Hereditas最新文献

{"title":"Identification and validation of USP15 and CUL2 as ubiquitination related biomarker in chronic obstructive pulmonary disease.","authors":"Shulei Sun, Zhaoxiong Zhang, Haiyan Zhao","doi":"10.1186/s41065-025-00460-1","DOIUrl":"10.1186/s41065-025-00460-1","url":null,"abstract":"<p><strong>Purpose: </strong>Ubiquitination is one of the important epigenetic modifications, influencing the development of various diseases. The objective of this study is to investigate the ubiquitination related genes in chronic obstructive pulmonary disease (COPD).</p><p><strong>Methods: </strong>The gene microarray dataset from COPD patients and ubiquitination related genes were analyzed. Venn diagram analysis was used to intersect differentially expressed genes and ubiquitination related genes. The functional enrichment analysis of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA) were performed on differentially expressed ubiquitination related genes. Finally, we confirmed the expression of hub genes through qPCR and western blot experiments in clinical COPD patients and cell lines.</p><p><strong>Results: </strong>We identified 2,932 differentially expressed genes and 96 differentially expressed ubiquitination related genes. GO analysis indicated that the differentially expressed ubiquitination related genes were mainly enriched in post-translational protein modification and ubiquitin ligase complex. KEGG analysis showed that ubiquitination related genes were mainly involved in ubiquitin mediated proteolysis and TNF signaling pathway. GSEA analysis suggested that some hub genes are involved in allograft rejection, IL6/JAK/STAT3 signaling and inflammatory response. Our qPCR and western blot experimental results indicate that the expression of USP15 and CUL2 is higher in COPD group compared to the control group, consistent with the bioinformatics analysis.</p><p><strong>Conclusion: </strong>Our bioinformatics analysis and experimental results suggest that USP15 and CUL2 may contribute to the progression of COPD through ubiquitination modification. To our knowledge, this is the first study to demonstrate the involvement of USP15 and CUL2 in COPD. Our results may provide new insights into the diagnosis and treatment of COPD.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"86"},"PeriodicalIF":2.7,"publicationDate":"2025-05-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12103031/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144142364","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 of LINC01158 in breast cancer and inhibition of proliferation and metastasis of breast cancer cells by regulating miR-711.","authors":"Xiaohe Lan, Zibai Guo, Linmei Lin, Wanqi Lin, Yi Zheng, Yabing Liu","doi":"10.1186/s41065-025-00452-1","DOIUrl":"10.1186/s41065-025-00452-1","url":null,"abstract":"<p><strong>Objective: </strong>Breast cancer (BC) has a poor prognosis due to metastasis and recurrence. LINC01158 is aberrantly expressed in breast cancer. Therefore, we investigated the regulatory mechanism and prognostic value of LINC01158 in BC.</p><p><strong>Methods: </strong>121 patients with BC were enrolled. LINC01158 and miR-711 levels were analyzed by RT-qPCR. Independent predictors of poor BC prognosis were analyzed by multifactorial Cox regression. Kaplan-Meier curves were used to analyze the 5-year survival rate of BC patients. DLR assay verified the relationship between LINC01158 and miR-711 target binding. CCK-8 was used to detect the proliferative capacity of cells. Transwell was used to analyze cell migration and invasion ability.</p><p><strong>Results: </strong>In BC tissues and cell lines, LINC01158 expression was reduced and miR-711 levels were elevated. Low expression of LINC01158 resulted in a shortened overall survival of BC patients. LINC01158 binds to the miR-711 target and negatively correlates with the level of miR-711. Overexpression of LINC01158 decreased miR-711 levels and reduced BC cell proliferation, migration and invasion. In addition, Cox regression results showed that LINC01158 was an independent prognostic factor for BC.</p><p><strong>Conclusion: </strong>LINC01158 may be a prognostic marker for BC. Increasing the expression level of LINC01158 could reduce the expression of miR-711, which could inhibit cell proliferation, migration and invasive behaviors, and has the potential to delay the progression of BC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"84"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127375","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":"Hsa_circ_0006837 suppresses gastric cancer cell proliferation, migration, and invasion via the modulation of miR-424-5p.","authors":"Yanxin He, Yeyu Sun, Yinglan Zheng, Yanfang Jiang, Na Li, Wenjie Zhao, Wanhua Ren","doi":"10.1186/s41065-025-00449-w","DOIUrl":"10.1186/s41065-025-00449-w","url":null,"abstract":"<p><strong>Background: </strong>The mechanism by which circRERE (hsa_circ_0006837) modulates the malignant progression of gastric cancer was investigated to identify a novel biomarker and therapeutic target for this disease.</p><p><strong>Methods: </strong>Hsa_circ_0006837 expression in GC tissues and cells was detected by RT-qPCR. Several data analysis methods were used to evaluate the significance of dysregulated hsa_circ_0006837 in GC. The patients were followed up for five years, and survival analysis was conducted using Kaplan-Meier curves. Cox regression was subsequently performed to analyze the risk factors for prognosis. The malignant behaviors of the cells were detected by the CCK-8 and Transwell assays. The relationship between hsa_circ_0006837 and miR-424-5p was assessed by conducting Spearman correlation analysis and verified by dual-luciferase reporter assay.</p><p><strong>Results: </strong>Hsa_circ_0006837 expression decreased in patients with GC, indicating a poorer patient prognosis. In GC cells, hsa_circ_0006837 overexpression suppressed malignant behaviors. Mechanistically, miR-424-5p was identified as a target of hsa_circ_0006837. The overexpression of miR-424-5p partially counteracted the suppressive effects of upregulated hsa_circ_0006837 on the malignant behaviors of GC cells. FBXO21 was identified as a downstream gene of the hsa_circ_0006837/miR-424-5p axis.</p><p><strong>Conclusions: </strong>To summarize, hsa_circ_0006837 is a biomarker for the prognosis of GC. Mechanistically, hsa_circ_0006837 overexpression can modulate the malignant behaviors of GC cells through miR-424-5p.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"85"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12100860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127295","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 m5C RNA modification-related gene signature for predicting prognosis and immune microenvironment-related characteristics of heart failure.","authors":"Zirui Liu, Rui Feng, Ying Xu, Meili Liu, Haocheng Wang, Yu Lu, Weiqi Wang, Jikai Wang, Cao Zou","doi":"10.1186/s41065-025-00454-z","DOIUrl":"10.1186/s41065-025-00454-z","url":null,"abstract":"<p><strong>Background: </strong>Methylation of RNA is involved in many pathophysiological processes. The roles of N6-methyladenosine (m6A) and N7-methylguanosine (m7G) in heart failure (HF) have been established. However, the impact of 5-methylcytosine (m5C) on HF and its relationship with the immune microenvironment (IME) remains elusive.</p><p><strong>Methods: </strong>GSE141910 (200 HF, 166 NFDs) was used as training cohort. Focusing on 9 identified m5C differently expressed genes (DEGs), random forests (RF), LASSO logistic regression, and SVM-RFE were employed to identify hub genes. ROC curves were plotted to confirm the predictive value in diagnostic model. ScRNA-seq revealed cell-type-specific m5C regulator expression patterns and HF IME. Hub genes were validated using HF rat models after myocardial infarction (MI) through quantitative reverse-transcription PCR (qRT-PCR) and western blot (WB). Consensus clustering algorithms identified two m5C-related HF subtypes. Single-sample gene-set enrichment analysis (ssGSEA) and CIBERSORT deconvolution algorithm analyzed the IME in HF. Finally, we employed WGCNA and PPI network to find m5C associated key genes and their clinical significance in HF subgroups.</p><p><strong>Results: </strong>In HF samples, four m5C regulators (NSUN6, DNMT3A, DNMT3B and ALYREF) were greatly upregulated, while five (NOP2, NSUN3, NSUN7, DNMT1 and TRDMT1) were downregulated compared to NFDs in the training set. ALYREF positively correlated with activated NK cells and monocytes, whereas TRDMT1 and NSUN3 showed inverse correlations with these cells. Four hub genes were identified by machine-learning algorithms and all verified by validation model. Single-cell RNA-seq dataset GSE183852 examined the levels of 13 m5C regulators across 11 different cell types in HF. In vivo experiments including qRT-PCR and WB finally identified NSUN6 as the most remarkable regulator. The diagnostic model demonstrated excellent performance in distinguishing between HF and NFDs (AUC 0.869, 95%CI 0.832-0.906). The two m5C subtypes exhibited distinct modification patterns, immune cell infiltration, immune checkpoints, and HLA gene expression. Additionally, 138 differentially expressed genes were uncovered based on m5C subtypes, and GSEA revealed associations with key pathophysiological mechanisms of HF. By using WGCNA and PPI network, three m5C associated key genes (RPS21, RPL36 and RPS19) were identified significantly influencing cardiac function in clinical practice.</p><p><strong>Conclusion: </strong>HF diagnostic model is developed based on 4 robust m5C RNA modification biomarkers (DNMT3B, NOP2, NSUN6 and DNMT1). Two distinct m5C RNA modification patterns in HF are identified, illustrating different IME characteristics. Our findings underline the significance of m5C regulators in HF, offering new perspectives on HF mechanisms and potential diagnostic and therapeutic strategies.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"83"},"PeriodicalIF":2.7,"publicationDate":"2025-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12096717/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127301","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":"Efficacy of red ointment in wound cavity repair following non-puerperal mastitis debridement.","authors":"Jiamei Feng, Zheng Chen, Jiaye Sun, Shijun Shao, Lu Xie, Wenchao Qu, Qingqian Gao, Xueqing Wu, Hua Wan","doi":"10.1186/s41065-025-00451-2","DOIUrl":"10.1186/s41065-025-00451-2","url":null,"abstract":"<p><strong>Background: </strong>The objective of this study is to evaluate the efficacy of red ointment, a widely used topical agent in traditional Chinese medicine, in promoting wound cavity repair following debridement for non-puerperal mastitis (NPM).</p><p><strong>Methods: </strong>A prospective, randomized controlled trial was conducted, including 88 patients diagnosed with NPM. Patients were randomly assigned to either the treatment group or the control group. All patients underwent debridement during the acute inflammatory phase. Postoperatively, the treatment group received daily dressing changes using sterile gauze strips infused with red ointment, whereas the control group received sterile gauze strips soaked in rivanol. The effectiveness of treatment was assessed after two weeks by evaluating the total effective rate, wound cavity score, symptom and sign score, laboratory parameters, and adverse events.</p><p><strong>Results: </strong>In the intention to treat analysis, the total effective rate was 90.9% in the red ointment group, which was higher than the 86.4% observed in the rivanol group. In the per protocol analysis, the total effective rate was 97.6% in the red ointment group, exceeding the 92.7% in the rivanol group. Compared with rivanol-treated gauze strips, the use of red ointment gauze strips resulted in a significantly greater reduction in wound cavity volume (p < 0.05), improved local breast symptoms (p < 0.05), and a lower wound cavity score (p < 0.001). Granulation tissue in the red ointment group exhibited a significantly fresher color compared to the rivanol group (p < 0.05). No significant differences were observed between the two groups regarding adverse effects on hepatic and renal function following treatment.</p><p><strong>Conclusion: </strong>The use of red ointment gauze strips for wound cavity filling following NPM debridement demonstrated favorable clinical efficacy and safety, providing a viable option for postoperative drainage management.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"82"},"PeriodicalIF":2.7,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12087160/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101771","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":"Novel exosome-associated LncRNA model predicts colorectal cancer prognosis and drug response.","authors":"Chi Zhou, Qian Qiu, Xinyu Liu, Tiantian Zhang, Leilei Liang, Yihang Yuan, Yufo Chen, Weijie Sun","doi":"10.1186/s41065-025-00445-0","DOIUrl":"10.1186/s41065-025-00445-0","url":null,"abstract":"<p><strong>Background: </strong>Exosomes are extracellular vesicles that carry various biological substances and have potential as functional mediators in cancers. However, little is known about special molecules in colorectal cancer (CRC) exosomes and their immunological functions.</p><p><strong>Aims: </strong>Using genomic data from the TCGA-CRC cohort, we constructed a prognostic model based on exosome-related lncRNA for the first time, and the biological role of MIR4713HG in CRC was deeply analyzed.</p><p><strong>Method: </strong>In this study, we downloaded the gene expression data and clinical data of CRC from the TCGA database. The limma package, SVM-REF and univariate Cox analysis were used to screen out core ERG (CERG) in CRC. LASSO and multivariate Cox regression analyses were used to filter out CERG-related LncRNA and construct a risk score. We explored the distribution and expression levels of ERG in immune cell types by scRNA-seq data. xCell was used to calculate the infiltration levels of stromal cells and immune cells in CRC. KM plotter was used for immunotherapy evaluation of core ERG. Next, we further provide colony formation assay, Transwell assay and xenograft models to understand the carcinogenic effect of MIR4713HG.</p><p><strong>Result: </strong>First, 43 differentially expressed ERG and 7 CERG were obtained. We explored the expression and distribution levels of CERG in 9 types of cells by scRNA-seq data. In addition, two key exosome-associated LncRNA (MIR4713HG and ZEB1-AS1) were obtained, and a risk score (EALncRI) was constructed. EALncRI could accurately predict the prognosis of CRC. Based on the EALncRI, we constructed a nomogram that is easy to use in clinical practice, which can more accurately and stably predict the prognosis of CRC patients. Furthermore, EALncRI was significantly correlated with the expression of 5 HLA molecules and 13 immune checkpoint molecules. MIR4713HG showed a good predictive effect in the overall survival of patients with immunotherapy evaluation. Knocking down the expression of MIR4713HG significantly inhibited proliferation and migration, and also impaired subcutaneous tumor growth in nude mice.</p><p><strong>Conclusion: </strong>In this study, a variety of machine learning algorithms were used to construct the EALncRI based on ERG, which can effectively predict the prognosis and distinguish the immune landscape of CRC. More importantly, we conducted an in-depth study on MIR4713HG, which may become an important therapeutic target in CRC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"79"},"PeriodicalIF":2.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12082951/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086151","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":"Curcumin alleviates LPS-induced WI-38 cell inflammation injury by regulating PTGS2 expression.","authors":"Hongli Xiao, Wangsheng Ma, Lin Zha, Yanmin Xiao, Hui Li","doi":"10.1186/s41065-025-00441-4","DOIUrl":"10.1186/s41065-025-00441-4","url":null,"abstract":"&lt;p&gt;&lt;strong&gt;Background: &lt;/strong&gt;Infantile pneumonia is a common infectious disease affecting infants and young children, which can lead to severe complications such as heart failure, significantly increasing morbidity and mortality rates among affected populations. Curcumin (CUR), a prominent natural polyphenol found in turmeric and other species of Curcuma, exhibits anti-inflammatory, antioxidant, and anticancer properties. Consequently, CUR has been hoped to be a therapeutic or preventive agent for several main human diseases. This study aims to explore the effects of CUR on lipopolysaccharide (LPS)-treated Wistsar Institute (WI)-38 cells.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Methods: &lt;/strong&gt;The cell vitality, proliferation, and apoptosis were assessed by cell counting kit-8 (CCK8) assay, 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry assays. Inflammation and oxidative stress were examined by measuring interleukins (IL)-6, IL-1β, tumor necrosis factor α (TNF-α), malondialdehyde (MDA), and superoxide dismutase (SOD) levels using the corresponding enzyme-linked immunosorbent assay (ELISA) test kits. The network pharmacology and molecule docking were carried out to predict the critical targets and potential therapeutic mechanisms of CUR in infantile pneumonia. The key target genes were predicted using PPI in the CUR protected-infantile pneumonia effect. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were employed to exhibit the biological function. The results of prediction were confirmed in vitro experiments.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Results: &lt;/strong&gt;LPS inhibited the vitality, proliferation, and SOD levels of WI-38 cells and facilitated the cell apoptosis, IL-6, IL-1β, TNF-α, and MDA levels. CUR abolished LPS-induced regulation WI-38 cell biological functions. Besides, the 16 hub genes from potential target genes of CUR and infantile pneumonia were screened. Moreover, six hub genes (enhanced green fluorescent protein (EGFP), v-akt murine thymoma viral oncogene homolog 1 (AKT1), prostaglandin endoperoxide synthase (PTGS2), signal transducer and activator of transcription 3 (STAT3), matrix metalloproteinase 9 (MMP9), and tumor necrosis factor (TNF)) in the CUR-protected-infantile pneumonia effect were identified by PPI analysis. The therapeutic effects of CUR on infantile pneumonia might relate to anti-viral and anti-inflammatory effects predicted by GO and KEGG enrichment analysis. Interestingly, CUR repressed LPS-stimulated facilitation of PTGS2 expression. The molecular docking demonstrated that PTGS2 could directly bind to CUR. The PTGS2 levels were inhibited by CUR treatment and negatively related to the time after WI-38 cells were treated with cycloheximide (CHX). PTGS2 knockdown could promote LPS-induced injury in WI-38 cells. CUR expedited cell vitality and proliferation and suppressed cell apoptosis, inflammation, and oxidative stress in LPS-induced WI-38 cells via down-regulating PTGS2.&lt;/p&gt;&lt;p&gt;&lt;strong&gt;Conclusion: &lt;/strong&gt;CUR attenu","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"81"},"PeriodicalIF":2.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086148","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":"Systematic evaluations of forensic effectiveness and genetic structures of two ethnic groups in Northwest China using a self-developed Multi-InDel panel.","authors":"Qinglin Liang, Qiong Lan, Qinglin Liu, Xiaolian Wu, Lisiteng Luo, Chunmei Shen, Bofeng Zhu","doi":"10.1186/s41065-025-00416-5","DOIUrl":"10.1186/s41065-025-00416-5","url":null,"abstract":"<p><strong>Background: </strong>The use of compound markers has gained significant interest among forensic practitioners, due to their ability to enhance genetic marker polymorphisms by introducing new alleles. Two or more closely linked insertion/deletion (InDel) markers form a compound marker termed Multi-InDel, which offers the advantages of microhaplotype (MH) and can be genotyped using capillary electrophoresis (CE) platform. A multiplex amplification panel, including 41 Multi-InDel markers and the sex-determination locus Amelogenin, was developed and validated as an effective tool for forensic and population genetics applications.</p><p><strong>Methods: </strong>A total of 245 Kazakh and Kyrgyz samples from China were genotyped based on the 41 Multi-InDel markers to evaluate the forensic efficacy of the panel. In addition, Multi-InDel genotyping data from 28 reference populations were collected, and population genetic analyses were performed to elucidate the genetic backgrounds of Chinese Kazakh and Kyrgyz groups.</p><p><strong>Conclusions: </strong>The Multi-InDel markers demonstrated high genetic polymorphisms in Chinese Kazakh and Kyrgyz ethnic groups, indicating their suitability for forensic applications. For the two ethnic groups, the cumulative power of discrimination (CPD) values were 0.999999999999999999999999835993 and 0.999999999999999999999999717184, respectively, while the cumulative power of exclusion (CPE) values were 0.999998887418153 and 0.999999348634116, respectively. Using this Multi-InDel panel, an average of 98.82% of full sibling (FS) pairs could be distinguished from unrelated individual pairs (likelihood ratio > 1). Regarding population genetics, Chinese Kazakh and Kyrgyz groups were found to exhibit an East Asia-Europe admixed ancestry pattern, while maintaining closer genetic affinities with East Asian populations.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"80"},"PeriodicalIF":2.7,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12083099/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086165","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":"WDR62 affects the progression of ovarian cancer by regulating the cell cycle.","authors":"Yuqi Yang, Wanting Jing, Lingqi Zhang, Yuhang Zhang, Ying Shang, Ye Kuang","doi":"10.1186/s41065-025-00444-1","DOIUrl":"https://doi.org/10.1186/s41065-025-00444-1","url":null,"abstract":"<p><strong>Background: </strong>Ovarian Cancer (OC) is a gynecological malignant tumor with an extremely high mortality rate, seriously endangering women's health. Due to its insidious clinical manifestations, most patients are diagnosed in the advanced stage of the disease. The currently clinically relied CA125 has limited specificity for the early diagnosis of ovarian cancer. Hence, identifying new promising biomarkers is crucial for the early screening, diagnosis, and treatment of ovarian cancer. Based on differential expression analysis, WGCNA and survival analysis, we identified a centromere-associated gene, WDR62, which is highly expressed in ovarian cancer and highly correlated with ovarian cancer, as well as the poor prognosis of ovarian cancer patients with high expression, suggesting that WDR62 may be a potential biomarker for ovarian cancer. Previous studies have shown that WDR62 is closely associated with the occurrence, development and prognosis of a variety of tumors. However, its role in ovarian cancer has not been studied in depth.</p><p><strong>Methods: </strong>Using combined TCGA and GTEx datasets from the UCSC database, along with WGCNA, and survival analysis, WDR62 was identified as a potential biomarker. GEPIA2 database, GEO database, qRT-PCR, and Western blot proved the expression of WDR62. Enrichment analysis, cell transfection, Western blots and CCK8 demonstrated the regulatory mechanism of WDR62, and the detailed mechanism of WDR62 involvement in the occurrence and development of ovarian cancer was predicted by interaction analysis and correlation analysis.</p><p><strong>Results: </strong>WDR62 was highly expressed in ovarian cancer cells compared to normal ovarian epithelial cells, both at the RNA and protein levels. Patients with high WDR62 expression had a poor survival prognosis. Upon WDR62 knockdown, the expression of cell cycle-related proteins CDK1 and C-Myc decreased in ovarian cancer cells, and the cell proliferative capacity was decreased. Based on bioinformatic analysis, it was hypothesized that WDR62 might mediate the JNK signaling pathway by interacting with MAPK8, thus affecting ovarian cancer progression through cell cycle regulation.</p><p><strong>Conclusions: </strong>WDR62 is overexpressed in ovarian cancer and is closely related to the prognosis of ovarian cancer patients. WDR62 promotes ovarian cancer progression by regulating the cell cycle and may influence its development through interaction with MAPK8 to mediate the JNK signaling pathway. These findings suggest that WDR62 could be a potential target for the early screening, diagnosis, and treatment of ovarian cancer.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"78"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12076949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077699","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":"Mechanistic insights into Circ-MBOAT2-mediated regulation of TLK1 through miR-664b-3p in non-small cell lung cancer.","authors":"DanTing Zhao, Cong Wang, GuangCheng Zhang, ZhengChang Song, ChunYu Luan","doi":"10.1186/s41065-025-00439-y","DOIUrl":"https://doi.org/10.1186/s41065-025-00439-y","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence highlights the critical involvement of dysregulated circular RNAs (circRNAs) in non-small cell lung cancer (NSCLC) pathogenesis. Nevertheless, the precise functional role and mechanistic contributions of circ-MBOAT2 in NSCLC remain poorly characterized. The purpose of this study was to investigate the pathogenesis of NSCLC based on circ-MBOAT2.</p><p><strong>Methods: </strong>Our investigation focused on the interplay among circ-MBOAT2, miR-664b-3p, and Tousled-like kinase 1 (TLK1) mRNA in NSCLC tissues, along with their association with the clinical and pathological characteristics of NSCLC patients. Sequences or plasmids were transfected into A549 cells. Gene expressions were identified using RT-qPCR and Western blot analysis. NSCLC cells' cancerous characteristics were identified using CCK-8, EdU, AnnexinV-PI double staining, and Transwell, while their in vivo growth was assessed through a xenografted tumor assay. To monitor alterations in the CD8⁺ T cell ratio and inflammatory factors in PBMCs, co-cultures were created with both normal human PBMCs and A549 cells. Evaluations using bioinformatics software, dual luciferase reporter tests, and RIP assays were performed to verify the connection between circ-MBOAT2 and miR-664b-3p, as well as the interaction between miR-664b-3p and TLK1.</p><p><strong>Results: </strong>Circ-MBOAT2 expression was up-regulated in NSCLC, and reducing circ-MBOAT2 hampered NSCLC cell proliferation, EMT, immune escape, and tumor growth in vivo. There was a negative correlation between miR-664b-3p expression and circ-MBOAT2, and miR-664b-3p could compete with circ-MBOAT2 for binding. miR-664b-3p downregulation impaired the anti-tumor effect of circ-MBOAT2 reduction on NSCLC cells. TLK1 expression was elevated in NSCLC specimens compared to adjacent normal tissues (p < 0.001), negatively correlated with miR-664b-3p (r=-0.351, p < 0.001), and positively correlated with circ-MBOAT2 (r = 0.341, p < 0.001). In vitro functional experiments showed that silencing TLK1 restrained NSCLC cell proliferation, EMT, and immune escape, whlie TLK1 overexpression rescued the inhibitory effects of miR-664b-3p on NSCLC cell malignant behaviors.</p><p><strong>Conclusion: </strong>Circ-MBOAT2 promotes NSCLC cell proliferation, EMT and immune escape by competitively binding to miR-664b-3p to promote TLK1 expression.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"77"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12076824/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077638","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}