Hereditas最新文献

{"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":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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}

{"title":"RNA-binding protein gene NOP58 exhibits crucial prognostic and therapeutic value in Ewing sarcoma.","authors":"Yannan Geng, Lu Yang, Rui Shao, Tiantong Xu, Lilong Zhang","doi":"10.1186/s41065-025-00440-5","DOIUrl":"https://doi.org/10.1186/s41065-025-00440-5","url":null,"abstract":"<p><strong>Background: </strong>Our aim was to identify crucial RNA-binding proteins (RBP) genes associated with Ewing sarcoma (EwS) in order to provide valuable insights into its mechanisms of tumorigenesis and to enhance therapeutic intervention.</p><p><strong>Results: </strong>Differential gene expression analysis identified candidate genes. Next, hub genes were generated by the results of protein-protein interaction (PPI) network, and univariate COX regression analysis. CIBERSORT was applied to analyze immune landscape. Furthermore, both in vitro and in vivo experiments were conducted to investigate the function of NOP58 in EwS.</p><p><strong>Results: </strong>A total of 179 RBP-related genes were significantly different in EwS tissues and normal controls. Among these, NOP58 ribonucleoprotein (NOP58) was considered as the hub gene, demonstrating significant prognostic value. Significantly, high NOP58 expression correlated with poor prognosis of EwS patients. Additionally, the levels of NOP58 were significantly up-regulated in EwS cells compared with human mesenchymal stem cells. Furthermore, knockdown of NOP58 notably inhibited the proliferation and migration of EwS cells. Moreover, NOP58 deficiency remarkably induced apoptosis and cell cycle arrest in EwS cells. In vivo studies on tumor-bearing mice demonstrated that NOP58 downregulation significantly inhibited tumor growth in EwS.</p><p><strong>Conclusion: </strong>Collectively, downregulation of NOP58 could inhibit the proliferation and migration of EwS cells in vitro and reduce murine xenograft tumor growth in vivo. These findings identified NOP58 as a promising regulator of EwS tumorigenesis, suggesting it may serve as a potential therapeutic target for EwS treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"76"},"PeriodicalIF":2.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12076867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144077696","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":"Integrated bioinformatic analysis identifies GADD45B as an immune-related prognostic biomarker in skin cutaneous melanoma.","authors":"Qing Zhang, Song He, Zhonghao Ji, Xiwen Zhang, Bao Yuan, Ruirui Liu, Yimin Yang, Yu Ding","doi":"10.1186/s41065-025-00437-0","DOIUrl":"https://doi.org/10.1186/s41065-025-00437-0","url":null,"abstract":"<p><p>Skin cutaneous melanoma (SKCM) arises from melanocytes and is an aggressive form of skin cancer. If left untreated, most melanomas will metastasize, posing a major health risk. GADD45B, a member of the GADD45 family, is known to be involved in DNA damage repair; however, its specific role in SKCM remains largely unclear. In this study, we comprehensively investigated the function of GADD45B in SKCM. By integrating 26 SKCM-related datasets from The Cancer Genome Atlas (TCGA), Cancer Cell Line Encyclopedia (CCLE), cBioPortal for Cancer Genomics (cBioPortal), Gene Expression Omnibus (GEO), and other databases, we conducted functional enrichment, immune infiltration, and single-cell analyses using R. Additionally, transcriptome sequencing of 30 human SKCM cell lines, phenotype characterization of 29 SKCM lines in vitro, and macrophage polarization analysis were performed. We found that GADD45B expression was significantly downregulated in SKCM patients compared to normal controls (p < 0.001), and higher GADD45B levels correlated with better prognosis (p < 0.05). GADD45B also showed high diagnostic accuracy, with an area under the curve (AUC) of 0.986. GO and KEGG analyses revealed a strong association between GADD45B and immune-related pathways. Gene Set Variation Analysis (GSVA) and single-cell sequencing suggested that GADD45B may serve as a novel immune checkpoint, predominantly expressed in macrophages and promoting M1 polarization. In vitro, overexpression of GADD45B significantly inhibited SKCM cell proliferation, potentially via suppression of the PI3K/Akt signaling pathway, and also reduced chemotherapy resistance. Furthermore, in vivo experiments using a xenograft mouse model demonstrated that GADD45B overexpression significantly suppressed tumor growth. Mice injected with GADD45B-overexpressing tumor cells exhibited smaller tumor volumes from day 15 onwards compared to controls, with markedly reduced tumor volume and weight at the endpoint. These results underscore the potential of GADD45B as an effective tumor suppressor in SKCM. In conclusion, our findings highlight GADD45B as a key regulator in SKCM progression, capable of restraining tumor cell proliferation and enhancing apoptosis. GADD45B holds promise as a novel diagnostic and prognostic biomarker and a potential target for SKCM immunotherapy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"74"},"PeriodicalIF":2.7,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967044","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":"Synergistic inhibition of gastric cancer cell proliferation by concanavalin A and silibinin via attenuation of the JAK/STAT3 signaling pathway and molecular docking analysis.","authors":"Gaoyan Hua, Lisha Zhao, Xianjing Zeng, Liang Luo","doi":"10.1186/s41065-025-00438-z","DOIUrl":"https://doi.org/10.1186/s41065-025-00438-z","url":null,"abstract":"<p><strong>Background: </strong>In the current period of pharmaceutical discovery, herbal remedies have shown to be an unmatched supply of anticancer medications. Plants and their derivatives, through analogues, play a vital role in cancer treatment.</p><p><strong>Objectives: </strong>The current investigation assessed the effectiveness of inhibiting the growth of gastric cancer cells in AGS cells by blocking the JAK/ STAT3 signalling pathways using the natural medicines Concanavalin A (Con-A) and silibinin (SB).</p><p><strong>Materials and methods: </strong>After being exposed to various doses of concanavalin A, and silibinin (Con-A + SB) for 24 h (0- 60 µM), the cells were evaluated for multiple studies. The MTT assay was used to examine the combination of Con-A + SB-induced cytotoxicity. To evaluate ROS, DCFH-DA staining was utilized. Dual (AO/EtBr) staining was performed to examine apoptotic modifications, and MMP levels in AGS cells were examined using the appropriate fluorescence staining assays. By using flow cytometry and western blotting, cell cycle, and apoptosis were assessed.</p><p><strong>Results: </strong>The relative cytotoxicity of Con-A and SB was found to be approximately 19.6 μM and 16.78 μM, (p < 0.05) correspondingly, according to the findings. After a 24-h incubation period, the combination of Con-A and SB generates significant cytotoxicity in AGS cells, with an IC₅₀ of 10.37 μM (p < 0.01). Furthermore, AGS cells treated with Con-A and SB concurrently showed increased apoptotic signals, exhibited by Bax overexpression, Bcl-2 downregulation, and Caspase-3 activation, as well as considerable ROS generation.</p><p><strong>Conclusion: </strong>Therefore, the combination usage of Con-A + SB has the potential to serve as a chemotherapeutic agent since it prevents the synthesis of JAK/STAT3 intermediated control of proliferation and cell cycle-regulating proteins.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"73"},"PeriodicalIF":2.7,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016915","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":"Predictive value of microRNA-133a-3p for early urinary incontinence after radical prostatectomy for prostate cancer and its correlation with rehabilitation effects.","authors":"Fan Yang, Qiuxia Qin, Juan Liu","doi":"10.1186/s41065-025-00443-2","DOIUrl":"https://doi.org/10.1186/s41065-025-00443-2","url":null,"abstract":"<p><strong>Aim: </strong>The present study was conducted with the objective ascertaining the clinical implication of microRNA-133a-3p (miR-133a-3p) for urinary incontinence (UI) and rehabilitation effects in prostate cancer after radical prostatectomy.</p><p><strong>Methods: </strong>The measurements of miR-133a-3p in urethral tissue samples from prostate cancer patients after radical prostatectomy were carried out via quantitative real-time polymerase chain reaction (qRT-PCR) detection. Receiver operation characteristic (ROC) curve and logistic regression analysis were employed for evaluating the predictive significance of miR-133a-3p for the early UI of prostate cancer patients with radical prostatectomy. Bioinformatics tools were employed for mining the miR-133a-3p possible genes.</p><p><strong>Results: </strong>An obvious reduction of miR-133a-3p was detected in patients with UI compared with those with urinary continence (UC) (P < 0.001), demonstrating a high diagnostic capacity for patients with UI. Moreover, miR-133a-3p could be an independent predictive index for the early UI in patients with prostate cancer after radical prostatectomy (P < 0.001). Additionally, urine miR-133a-3p was notably increased in the UI patients after rehabilitation (P < 0.001). MiR-133a-3p largely concentered on the muscle-related diseases pathways using bioinformatics tools.</p><p><strong>Conclusion: </strong>MiR-133a-3p was a promising indicator for predicting early UI in patients with prostate cancer after radical prostatectomy.</p><p><strong>Clinical trial number: </strong>Not applicable.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"75"},"PeriodicalIF":2.7,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12067700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143964228","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":"Circ_RPPH1 promotes bladder urothelium carcinoma proliferation and EMT by recruiting and binding to EIF4 A3.","authors":"HuaWei Liu, JunMin Ma, Xia Yan","doi":"10.1186/s41065-025-00442-3","DOIUrl":"https://doi.org/10.1186/s41065-025-00442-3","url":null,"abstract":"<p><strong>Background: </strong>The involvement of circ_RPPH1 in bladder urothelial carcinoma (BUC) remains unclear, as well as the underlying mechanism.</p><p><strong>Methods: </strong>Circ_RPPH1 levels in BUC cells and tissues were measured via RT-qPCR. Downregulation of circ_RPPH1 was assessed using colony formation, CCK-8, wound healing, and Transwell assays to evaluate proliferation, migration, and invasion. RIP and RNA pull-down confirmed circ_RPPH1 binding to EIF4A3, while immunoblotting analyzed EIF4A3 and EMT-related proteins.</p><p><strong>Results: </strong>High circ_RPPH1 levels in BUC correlated with tumor invasion depth. Its knockout suppressed proliferation, invasion, and EMT, while circ_RPPH1 overexpression reduced EIF4A3 binding to N-cadherin and Vimentin mRNA, promoting EMT.</p><p><strong>Conclusion: </strong>Circ_RPPH1 promotes tumor growth and EMT in BUC by inhibiting EIF4A3-mediated mRNA regulation, activating the EIF4A3/N-cadherin/Vimentin pathway.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"72"},"PeriodicalIF":2.7,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12065329/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143989051","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 miR-6515-5p in predicting diagnosis and prognosis for acute respiratory distress syndrome suffering from pulmonary fibrosis.","authors":"Xueqin Huang, Peng Xu, Guangwen Long, Feihong Huang, Qian Zhang, Xiulin Yang, Hongpeng Sun, Chunling Ji, Wang Liu","doi":"10.1186/s41065-025-00436-1","DOIUrl":"https://doi.org/10.1186/s41065-025-00436-1","url":null,"abstract":"<p><strong>Background: </strong>The high mortality rate of ARDS is closely related to pulmonary fibrosis (PLF), and the degree of pulmonary fibrosis affects the prognosis of ARDS. Numerous studies indicated the abnormal expression of miRNAs in the pathogenesis of various lung diseases, such as ARDS and PLF. This study aimed to explore the expression of serum miR-6515-5p and its clinical performance in ARDS complicated with PLF.</p><p><strong>Methods: </strong>RT-qPCR analysis was employed to measure miR-6515-5p levels within the serum specimens from ARDS patients who either had PLF or did not. Receiver Operating Characteristics (ROC) curve was conducted to evaluate the diagnostic value of miR-6515-5p. To analyze the risk factors linked with the development of PLF in ARDS patients, logistic regression analysis was conducted. Kaplan-Meier curve was conducted to assess the prognostic value of miR-6515-5p in predicting the outcome of ARDS patients with PLF. Multivariate COX regression analysis was performed to identify the PLF-related risk factors associated with outcomes.</p><p><strong>Results: </strong>Serum miR-6515-5p was downregulated in ARDS patients, especially in patients suffering from PLF. miR-6515-5p expression can distinguish ARDS patients from healthy individuals and related to the occurrence of PLF. Most patients with low miR-6515-5p expression had low FVC and DLCO, as well as high Murray score and APACHE II score. Moreover, miR-6515-5p expression has a certain high value in differentiating ARDS patients with PLF from those without PLF. In addition, miR-6515-5p may be a prognostic marker in ARDS patients suffering from PLF.</p><p><strong>Conclusions: </strong>These data identified the abnormal expression of miR-6515-5p in ARDS and PLF, and implied a potential clinical early diagnostic and prognostic marker in ARDS suffering from PLF.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"71"},"PeriodicalIF":2.7,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12034141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143985251","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}