Hereditas最新文献

筛选
英文 中文
Managing gastrointestinal involvement in cutaneomucosal venous malformation: safety and efficacy of endoscopic sclerotherapy. 处理皮肤粘膜静脉畸形的胃肠道受累:内镜硬化治疗的安全性和有效性。
IF 2.5 3区 生物学
Hereditas Pub Date : 2025-06-23 DOI: 10.1186/s41065-025-00486-5
Jiaxue Zhu, Wei Liu, Zehua Zhang, Bensong Duan, Xiaohan Yan
{"title":"Managing gastrointestinal involvement in cutaneomucosal venous malformation: safety and efficacy of endoscopic sclerotherapy.","authors":"Jiaxue Zhu, Wei Liu, Zehua Zhang, Bensong Duan, Xiaohan Yan","doi":"10.1186/s41065-025-00486-5","DOIUrl":"10.1186/s41065-025-00486-5","url":null,"abstract":"<p><p>Blue rubber bleb nevus syndrome (BRBNS) and cutaneomucosal venous malformation (VMCM) both manifest as venous malformations (VMs) characterized by blue, compressible nodules. While BRBNS typically involves visceral organs, particularly the gastrointestinal (GI) tract, VMCM has conventionally been considered to spare internal organs. Our findings, however, reveal that VMCM can indeed extend to the GI system and demonstrate that endoscopic sclerotherapy is safe and effective for its management. This underscores the importance of genetic testing and systemic evaluation in patients with multifocal VMs, suggesting the need for revised diagnostic criteria and a more nuanced approach to classification of these disorders.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"113"},"PeriodicalIF":2.5,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12186395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475050","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}
引用次数: 0
Early arteriovenous malformation mimicking pediatric capillary malformation: diagnostic value of infrared thermography. 早期动静脉畸形模拟儿童毛细血管畸形:红外热成像的诊断价值。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-23 DOI: 10.1186/s41065-025-00484-7
Hao Gu, Xiaojie Yue, Xiong Zhao, Qiang Shu
{"title":"Early arteriovenous malformation mimicking pediatric capillary malformation: diagnostic value of infrared thermography.","authors":"Hao Gu, Xiaojie Yue, Xiong Zhao, Qiang Shu","doi":"10.1186/s41065-025-00484-7","DOIUrl":"10.1186/s41065-025-00484-7","url":null,"abstract":"<p><p>Early-stage arteriovenous malformations (AVMs) and port-wine stains (PWS) exhibit overlapping clinical presentations, notably as flat, irregular erythema, posing significant diagnostic challenges. Conventional imaging techniques offer insufficient resolution for microvascular assessment during initial evaluation, and definitive diagnosis requires invasive tissue biopsy. We report a case of a 4-year-old boy initially misdiagnosed with facial PWS following ineffective photodynamic therapy. Digital images with quantitive readings acquired by infrared thermography (IRT) camera detected localized hyperthermia within the lesion, indicative of underlying hemodynamic anomalies. Skin biopsy of the lesion was performed and a somatic KARS mutation (p. Gln61His) was detected via targeted sequencing. Subsequent digital subtraction angiography confirmed the presence of micro-arteriovenous fistulas, thereby confirming the diagnosis of early AVM. This case illustrates the clinical utility of IRT in detecting subtle temperature variations associated with vascular pathophysiology. Integrating IRT into initial diagnostic algorithms may enhance the accuracy of differential diagnosis for vascular malformations, particularly early-stage AVMs.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"112"},"PeriodicalIF":2.7,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183846/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475048","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}
引用次数: 0
Exploring the potential mechanisms of m6A modification in septic acute respiratory distress syndrome: a bioinformatics analysis. 探讨m6A修饰在脓毒性急性呼吸窘迫综合征中的潜在机制:生物信息学分析。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-23 DOI: 10.1186/s41065-025-00480-x
Shaoyang Zhang, Qinghui Fu, Zhipeng Xu, Mingjie Fu, Jianfeng Zhao, Wenqiao Yu
{"title":"Exploring the potential mechanisms of m6A modification in septic acute respiratory distress syndrome: a bioinformatics analysis.","authors":"Shaoyang Zhang, Qinghui Fu, Zhipeng Xu, Mingjie Fu, Jianfeng Zhao, Wenqiao Yu","doi":"10.1186/s41065-025-00480-x","DOIUrl":"10.1186/s41065-025-00480-x","url":null,"abstract":"<p><strong>Background: </strong>Acute respiratory distress syndrome (ARDS) remains a leading cause of mortality in intensive care units. The N6-methyladenosine (m6A) mRNA modification is critical in various pathological conditions, yet its role in the ARDS microenvironment, particularly at the single-cell level, remains poorly understood.</p><p><strong>Methods: </strong>Single-cell and bulk RNA-sequencing datasets were sourced from the GEO databases. Bioinformatics and experimental approaches were employed to investigate the associations between m6A regulators and hub genes in ARDS.</p><p><strong>Results: </strong>WTAP, HNRNPA2B1, and HNRNPC exhibited extensive expression within the ARDS microenvironment. Consensus clustering analysis segregated patients with sepsis into distinct subgroups, with WTAP showing significant variation across these groups. Weighted gene co-expression network analysis (WGCNA) identified the brown module as most associated with WTAP, revealing five hub genes. Validation experiments confirmed high expression levels of WTAP and MYC in lung tissues. Functional assays further demonstrated that WTAP enhances ARDS progression.</p><p><strong>Conclusions: </strong>In conclusion, bioinformatics analysis and preliminary experimental data suggest that WTAP promotes ARDS onset and progression by regulating m6A methylation and facilitating immune cell infiltration.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"111"},"PeriodicalIF":2.7,"publicationDate":"2025-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12183920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144475049","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}
引用次数: 0
Mechanism of LINC00958 in ferroptosis of breast cancer through the SRSF1/GPX4 axis. LINC00958通过SRSF1/GPX4轴参与乳腺癌铁下垂的机制。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-19 DOI: 10.1186/s41065-025-00469-6
Shan Wang, Xinlu Liu, Xiaoli Hou, Wei Sun, Jiajie Chen, Yasen Cao, Hong Cheng
{"title":"Mechanism of LINC00958 in ferroptosis of breast cancer through the SRSF1/GPX4 axis.","authors":"Shan Wang, Xinlu Liu, Xiaoli Hou, Wei Sun, Jiajie Chen, Yasen Cao, Hong Cheng","doi":"10.1186/s41065-025-00469-6","DOIUrl":"10.1186/s41065-025-00469-6","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"110"},"PeriodicalIF":2.7,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12180173/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144333008","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}
引用次数: 0
Epithelial zinc finger protein in lung adenocarcinoma: prognostic biomarker with molecular and clinical implications. 肺腺癌上皮锌指蛋白:具有分子和临床意义的预后生物标志物。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-18 DOI: 10.1186/s41065-025-00476-7
Xiaofen Wen, Jianling Zhu, Didi Xi, Minna Chen, De Zeng, Wenwu Xue, Danxia Lin, Jiaxin Shen
{"title":"Epithelial zinc finger protein in lung adenocarcinoma: prognostic biomarker with molecular and clinical implications.","authors":"Xiaofen Wen, Jianling Zhu, Didi Xi, Minna Chen, De Zeng, Wenwu Xue, Danxia Lin, Jiaxin Shen","doi":"10.1186/s41065-025-00476-7","DOIUrl":"10.1186/s41065-025-00476-7","url":null,"abstract":"<p><strong>Objective: </strong>This study aimed to evaluate the prognostic significance of epithelial zinc finger protein (EZF/KLF4) in lung adenocarcinoma (LAC) and explore its potential roles in tumor progression and immune regulation.</p><p><strong>Methods and materials: </strong>EZF expression and its associations with clinical characteristics were analyzed using TCGA and GEO datasets, and validated by immunohistochemistry in 25 paired LAC and adjacent normal tissues. Mechanistic insights were investigated through protein-protein interaction networks, gene set enrichment analysis (GSEA), DNA methylation profiling, and immune cell infiltration analysis via single-sample GSEA. A prognostic nomogram incorporating EZF expression, pT and pN stages, and residual tumor status was constructed using Cox regression modeling.</p><p><strong>Results: </strong>EZF expression was significantly downregulated in LAC tissues compared to normal tissues across multiple cohorts (P < 0.001), yet paradoxically associated with advanced tumor stages and worse overall, disease-specific, and progression-free survival. Functional analyses revealed EZF-associated pathways enriched in immune modulation. EZF expression correlated strongly with infiltrating immune cells, including NK cells, eosinophils, mast cells, and neutrophils. Hypomethylation of the EZF promoter was linked to poor prognosis. The constructed nomogram exhibited strong predictive accuracy for patient outcomes.</p><p><strong>Conclusion: </strong>EZF functions as a context-dependent regulator in LAC and may act as a prognostic biomarker by modulating tumor-immune interactions. These findings offer novel insights into the integration of molecular and immune features for personalized risk stratification and therapeutic guidance in LAC.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"106"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175355/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325316","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}
引用次数: 0
circ-NOLC1 inhibits the development of cervical cancer by regulating miR-330-5p-PALM signaling axis. circ-NOLC1通过调节miR-330-5p-PALM信号轴抑制宫颈癌的发展。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-18 DOI: 10.1186/s41065-025-00478-5
Yali Duo, Cong Kang, Lei Zheng, Jing Wang, Zhongjie Liu, FengLing Bi, Lei Qiu, Ning Zhao
{"title":"circ-NOLC1 inhibits the development of cervical cancer by regulating miR-330-5p-PALM signaling axis.","authors":"Yali Duo, Cong Kang, Lei Zheng, Jing Wang, Zhongjie Liu, FengLing Bi, Lei Qiu, Ning Zhao","doi":"10.1186/s41065-025-00478-5","DOIUrl":"10.1186/s41065-025-00478-5","url":null,"abstract":"<p><strong>Background: </strong>Recent studies have increasingly demonstrated that circular RNAs (circRNAs) play significant roles in the occurrence and progression of cervical cancer (CC). In CC, circRNAs act as ceRNAs by sponging miRNAs to regulate genes associated with proliferation, migration, and apoptosis, exhibiting both promoting and inhibiting effects on tumor progression. The aim of this study was to clarify the role of hsa_circ_0019686 (named circ-NOLC1) in CC.</p><p><strong>Methods: </strong>By conducting an online GEO2R analysis of the expression profile GSE113696 in the GEO database, circ-NOLC1 was selected. The expression levels of circ-NOLC1 in CC cell lines were measured using real-time quantitative PCR (RT-qPCR). The role of circ-NOLC1 in CC was validated through both in vitro and in vivo gain-of-function assays. Bioinformatic analysis, combined with luciferase reporter and RNA Immunoprecipitation (RIP) assays, confirmed that circ-NOLC1 acts as a sponge for miR-330-5p and regulates the expression of paralemmin-1 (PALM). The role of the circ-NOLC1-miR-330-5p-PALM signaling axis in CC was elucidated through the rescue experiments. Relative gene expression levels were measured using RT-qPCR, while relative protein levels were assessed through immunohistochemistry (IHC). CCK-8, wound healing, Transwell, and flow cytometry assays were employed to evaluate CC cell proliferation, migration, and invasion, respectively.</p><p><strong>Results: </strong>The expression levels of circ-NOLC1 were dramatically downregulated in CC cells (P < 0.001). Up-regulation of circ-NOLC1 significantly inhibited cell proliferation (P < 0.001), migration (P < 0.01) and invasion (P < 0.01), while promoting cell apoptosis (P < 0.001). In vivo studies showed that up-regulation of circ-NOLC1 suppressed tumor growth (tumor volume: P < 0.001; tumor weight: P < 0.01). Additionally, miR-330-5p was found to be up-regulated in CC (P < 0.001), whereas PALM was downregulated in CC (P < 0.001). The up-regulation of circ-NOLC1 inhibited the expression of miR-330-5p (P < 0.001) and enhanced the expression of PALM (P < 0.001). Rescue experiments further demonstrated that the up-regulation of circ-NOLC1 inhibited CC cell proliferation (P < 0.001), migration (P < 0.001), invasion (P < 0.001), while promoting apoptosis (P < 0.001) through the regulation of the miR-330-5p-PALM pathway.</p><p><strong>Conclusion: </strong>The circ-NOLC1 inhibits CC development through regulating the miR-330-5p-PALM signaling axis. This finding reveals a novel mechanism and identifies potential therapeutic targets, emphasizing the necessity for further regulatory studies and clinical validation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"108"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175339/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325315","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}
引用次数: 0
Ilizarov-assisted periosteal distraction for refractory arteriovenous malformation ulcers: first clinical report in Asia. ilizarov辅助骨膜撑开治疗难治性动静脉畸形溃疡:亚洲首个临床报告。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-18 DOI: 10.1186/s41065-025-00479-4
Xiangyi Wu, Ren Cai, Mao Ye, Xitao Yang, Dachuan Sun, Yifeng Han, Xindong Fan, Jiaxue Zhu
{"title":"Ilizarov-assisted periosteal distraction for refractory arteriovenous malformation ulcers: first clinical report in Asia.","authors":"Xiangyi Wu, Ren Cai, Mao Ye, Xitao Yang, Dachuan Sun, Yifeng Han, Xindong Fan, Jiaxue Zhu","doi":"10.1186/s41065-025-00479-4","DOIUrl":"10.1186/s41065-025-00479-4","url":null,"abstract":"<p><p>Refractory ulcers caused by high-flow arteriovenous malformations (AVMs) pose significant therapeutic challenges due to persistent tissue ischemia and shear stress-induced graft failure. Traditional embolization or flap reconstruction strategies often yield suboptimal outcomes, particularly in weight-bearing regions. We present a 28-year-old female with a non-healing dorsal foot AVM ulcer despite multiple embolizations and radical toe amputations. Genetic testing revealed a KRAS mutation, confirming a somatic etiology of AVM. After a debridement and local flap repair, we employed Ilizarov-assisted periosteal distraction to improve local perfusion. 75% of the wound epithelialized and the infection resolved within 4 weeks postoperatively, with granulation tissue covering the remainder. This case highlights the mechanobiological advantages of Ilizarov-based neovascular stimulation in AVM-related ischemic ulcers.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"107"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175424/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325317","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}
引用次数: 0
Abnormal expression of miR-330-3p predicts post-prostatectomy urinary incontinence and regulates the function of urethral fibroblasts by targeting MMP2. miR-330-3p异常表达可预测前列腺切除术后尿失禁,并通过靶向MMP2调控尿道成纤维细胞功能。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-18 DOI: 10.1186/s41065-025-00475-8
Xiaoying Feng, Yuanyuan Mi, Mengye Weng
{"title":"Abnormal expression of miR-330-3p predicts post-prostatectomy urinary incontinence and regulates the function of urethral fibroblasts by targeting MMP2.","authors":"Xiaoying Feng, Yuanyuan Mi, Mengye Weng","doi":"10.1186/s41065-025-00475-8","DOIUrl":"10.1186/s41065-025-00475-8","url":null,"abstract":"<p><strong>Background: </strong>Post-prostatectomy urinary incontinence (PPUI) is a common complication for patients with prostate cancer after surgery. MicroRNA-330-3p (miR-330-3p) is down-regulated in stress urinary incontinence patients. However, its clinical role and regulatory mechanism in PPUI remain unknown.</p><p><strong>Objective: </strong>To assess the clinical significance of miR-330-3p in PPUI and to explore the potential mechanisms via matrix metalloproteinase 2 (MMP2) regulation.</p><p><strong>Methods: </strong>This study enrolled 135 ageing prostate cancer patients (86 without PPUI, 49 with PPUI). Reverse transcription PCR (RT-qPCR) was utilized to measure the levels of miR-330-3p, while Receiver operating characteristic (ROC) analysis was conducted to evaluate the predictive significance of miR-330-3p for PPUI. The proliferative of human urethral fibroblasts (HUFs) was assessed by Cell Counting Kit-8 (CCK-8) assay, while inflammatory cytokines were quantified via enzyme-linked immunosorbent assay (ELISA) kits. Western blot assay was employed to examine the protein levels of extracellular matrix (ECM) remodeling-related markers. The miR-330-3p/MMP2 interaction was validated by dual-luciferase assay.</p><p><strong>Result: </strong>miR-330-3p was significantly downregulated in PPUI patients, with low expression predicting PPUI. In HUFs, miR-330-3p overexpression inhibited IL-1β-induced hyperproliferation, inflammation, and ECM degradation. Overexpression of MMP2 counteracted the influence of miR-330-3p mimic on HUFs.</p><p><strong>Conclusion: </strong>miR-330-3p is a potential biomarker for PPUI and regulates the function of urethral fibroblasts by targeting MMP2.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"109"},"PeriodicalIF":2.7,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12175350/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325314","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}
引用次数: 0
Prognostic analysis of bladder cancer with neddylation-related genes. 与泛素化相关基因的膀胱癌预后分析。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-16 DOI: 10.1186/s41065-025-00463-y
Huang Xiaolong, Deng Min, Zhang Sizhou, Hu Daorong, Pan Juncheng, Wang Yanjian, Li Jie Gu Hong, Zheng Ji, Wu Qingjian
{"title":"Prognostic analysis of bladder cancer with neddylation-related genes.","authors":"Huang Xiaolong, Deng Min, Zhang Sizhou, Hu Daorong, Pan Juncheng, Wang Yanjian, Li Jie Gu Hong, Zheng Ji, Wu Qingjian","doi":"10.1186/s41065-025-00463-y","DOIUrl":"10.1186/s41065-025-00463-y","url":null,"abstract":"<p><strong>Background: </strong>Previous studies have demonstrated a close association between neddylation modifications and tumor progression as well as alterations in the microenvironment. This study aimed to explore the role of neddylation in bladder cancer (BLCA) progression and its prognostic significance.</p><p><strong>Methods: </strong>Gene expression data from the TCGA database were analyzed to identify neddylation gene modules using the limma software package and weighted gene co-expression network analysis (WGCNA). Prognostic models based on neddylation-related genes were subsequently developed through LASSO and Cox regression analyses. Additionally, a protein-protein interaction (PPI) network, gene set enrichment analysis (GSEA), and BLCA single-cell sequencing data were utilized to explore the functional roles of hub genes in BLCA and their impact on biological pathways. The expression of these hub genes was further validated in clinical samples via RT-qPCR.</p><p><strong>Results: </strong>WGCNA analysis revealed 1412 neddylation-related hub genes. LASSO and Cox regression analyses subsequently identified six key genes: CUL1, PUM2, UBE2D3, HIF3A, COPS2, and DDB1. Transcriptomic data and RT-qPCR findings indicated that PUM2 and HIF3A exhibited high expression levels in normal tissues, while DDB1 showed increased expression in tumor tissues; no significant changes were observed for CUL1, COPS2, and UBE2D3. By integrating these gene expressions with significant clinical features, a prognostic model was constructed that demonstrated excellent diagnostic efficiency (AUC: 0.793 at 1 year, 0.792 at 3 years, and 0.773 at 5 years). In addition, single cell sequencing highlighted the potential role of these genes in modulating immune responses and mediating interactions between tumor cells and immune cells. GSEA also suggested that DDB1 may play a crucial role in orchestrating key biological processes associated with BLCA, particularly in activating apoptotic signaling pathways.</p><p><strong>Conclusion: </strong>The six neddylation-related genes (CUL1, PUM2, UBE2D3, HIF3A, COPS2, and DDB1) emerge as potential independent indicators of survival in patients with BLCA, and the constructed survival models exhibit significant diagnostic efficacy.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"105"},"PeriodicalIF":2.7,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12172356/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144309861","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}
引用次数: 0
MiR-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway. MiR-106b-5p通过抑制TGF-β/Smad通路改善慢性肾脏疾病的进展。
IF 2.7 3区 生物学
Hereditas Pub Date : 2025-06-13 DOI: 10.1186/s41065-025-00468-7
Qihao Ma, Li Xu, Peng Zhou, Bo Yang, Yong Li, Danan Sun
{"title":"MiR-106b-5p improving the progression of chronic kidney disease by inhibiting the TGF-β/Smad pathway.","authors":"Qihao Ma, Li Xu, Peng Zhou, Bo Yang, Yong Li, Danan Sun","doi":"10.1186/s41065-025-00468-7","DOIUrl":"https://doi.org/10.1186/s41065-025-00468-7","url":null,"abstract":"<p><strong>Background: </strong>Chronic Kidney Disease (CKD) is a progressive disorder marked by renal impairment and declining kidney function.</p><p><strong>Aims: </strong>To investigate the expression of miR-106b-5p in CKD and its regulatory relationship with the TGF-β/Smad pathway.</p><p><strong>Methods: </strong>A total of 150 cases of CKD patients were selected as the observation group, while 100 healthy individuals served as the control group. Lipopolysaccharide (LPS) was utilized to induce damage to HK-2 cells. Real-time fluorescence PCR was used to detect the expression of genes. The CCK - 8 assay was utilized to evaluate cell proliferation, while flow cytometry was applied to measure the cell apoptosis rate.</p><p><strong>Results: </strong>miR-106b-5p is notably downregulated in CKD and exhibits a significant positive correlation with the eGFR in affected patients. Additionally, miR-106b-5p demonstrates a strong association with the levels of inflammatory factors in individuals with CKD. Furthermore, the expression of miR-106b-5p is reduced in LPS-induced HK-2 cells. Upregulation of miR-106b-5p can improve the inhibitory effect of LPS on the viability of HK-2 cells, reduce the apoptosis rate of cells, and alleviate the inflammatory response. miR-106b-5p serves as a negative regulatory factor within the TGF-β/Smad signaling pathway by directly targeting the pivotal receptor TGFBR2 and the downstream effectors SMAD2/3 within the TGF-β signaling cascade.</p><p><strong>Conclusions: </strong>miR-106b-5p ameliorates CKD progression by suppressing the TGF - β/Smad signaling pathway and could potentially be a therapeutic target for CKD.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"162 1","pages":"103"},"PeriodicalIF":2.7,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12164090/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293639","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}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信