DNA and cell biology最新文献

Utilizing Long-Read Sequencing for Haplotype Construction and Prevention of Autosomal Dominant Polycystic Kidney Disease Transmission in Mosaicism Family.

DNA and cell biology Pub Date : 2025-04-02 DOI: 10.1089/dna.2024.0280

Wu Zubo, Jie Liu, Yi Liu, Xiaoli Wang, Defeng Shu

{"title":"Utilizing Long-Read Sequencing for Haplotype Construction and Prevention of Autosomal Dominant Polycystic Kidney Disease Transmission in Mosaicism Family.","authors":"Wu Zubo, Jie Liu, Yi Liu, Xiaoli Wang, Defeng Shu","doi":"10.1089/dna.2024.0280","DOIUrl":"https://doi.org/10.1089/dna.2024.0280","url":null,"abstract":"This study presents a case of autosomal dominant polycystic kidney disease (ADPKD) involving a mosaic microdeletion in the PKD1 gene and explores the application of long-read sequencing technologies for haplotype construction and preimplantation genetic testing (PGT). We report on a family where the proband was clinically diagnosed with PKD and found to have a partial deletion of the PKD1 gene because of the mosaic deletion mutation of PKD1 in the mother of the proband. Utilizing Oxford Nanopore long-read sequencing, we successfully constructed the haplotype of the deleted fragment region and identified an unaffected embryo for transplantation, resulting in a successful pregnancy. The prenatal genetic diagnosis confirmed the absence of deletion abnormalities in the fetus. Our findings underscore the significance of integrating advanced genomic technologies into clinical practice for PGT in ADPKD, particularly in cases involving partial deletion of X chromosome mosaic embryo transferred or complex structural variants. This approach not only prevents the transmission of ADPKD but also demonstrates the utility of long-read sequencing in overcoming the limitations of traditional PGT methods. Further research is warranted to evaluate the broader application of long-read sequencing for other monogenic disorders and to refine these techniques for enhanced diagnostic precision and clinical outcomes.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143775044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Liquiritin as a Tumor Suppressor Prevents the Development of Breast Cancer via the Epidermal Growth Factor Receptor/Mitogen-Activated Protein Kinase 8 Signaling Pathway.

DNA and cell biology Pub Date : 2025-04-01 Epub Date: 2025-02-27 DOI: 10.1089/dna.2024.0249

Ping Li, Lili Yuan, Ying Jiang, Yue Chen, Manyu Zhang, Ling Jiang, Pengling Ge

{"title":"Liquiritin as a Tumor Suppressor Prevents the Development of Breast Cancer via the Epidermal Growth Factor Receptor/Mitogen-Activated Protein Kinase 8 Signaling Pathway.","authors":"Ping Li, Lili Yuan, Ying Jiang, Yue Chen, Manyu Zhang, Ling Jiang, Pengling Ge","doi":"10.1089/dna.2024.0249","DOIUrl":"10.1089/dna.2024.0249","url":null,"abstract":"Liquiritin, a key component extracted from Glycyrrhiza radix, exhibits a variety of physiological effects. This study investigates the role of liquiritin in the progression of breast cancer. This investigation conducted experiments using two breast cancer cell lines treated with varying concentrations of liquiritin, further validating our findings in vivo. Bioinformatics analysis was used to identify the pathways potentially regulated by liquiritin in breast cancer. The results indicated that the epidermal growth factor receptor (EGFR) and mitogen-activated protein kinase 8 (MAPK8) are potential downstream factors regulated by liquiritin in breast cancer. Our findings demonstrated that liquiritin significantly suppressed cell proliferation and induced cell cycle arrest in a dose-dependent manner. In addition, liquiritin triggered apoptosis by inhibiting the phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B signaling pathway. Liquiritin also reduced mitochondrial membrane potential, leading to mitochondrial dysfunction and promoting excessive reactive oxygen species (ROS) production by suppressing the EGFR/MAPK8 signaling pathway. Furthermore, liquiritin treatment resulted in a notable decrease in tumor size in breast cancer models through inhibiting cell proliferation and promoting apoptosis. In conclusion, liquiritin serves as an effective tumor suppressor, suppressing the proliferation and cell cycle progression of breast cancer cells, while inducing apoptosis by regulating mitochondrial function and ROS generation via the EGFR/MAPK8 signaling pathway.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"197-208"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inhibition of CCN5 Protects Against Apoptosis and Endoplasmic Reticulum Stress in Bisphenol A-Induced Sertoli Cells via p38/JNK MAPK Signaling Pathway.

DNA and cell biology Pub Date : 2025-04-01 Epub Date: 2025-02-26 DOI: 10.1089/dna.2024.0247

Lijiang Zhao, Xueqing Wu, Qiang Li, Yan Shen, Sheng Zeng, Jinbao Wang, Qian Liu

{"title":"Inhibition of CCN5 Protects Against Apoptosis and Endoplasmic Reticulum Stress in Bisphenol A-Induced Sertoli Cells via p38/JNK MAPK Signaling Pathway.","authors":"Lijiang Zhao, Xueqing Wu, Qiang Li, Yan Shen, Sheng Zeng, Jinbao Wang, Qian Liu","doi":"10.1089/dna.2024.0247","DOIUrl":"https://doi.org/10.1089/dna.2024.0247","url":null,"abstract":"Bisphenol A (BPA) is the most common endocrine disruptor that has toxicity to the reproductive system and male infertility. However, the underlying mechanisms of BPA's toxicity to Sertoli cells remain poorly understood. Cellular communication network factor 5 (CCN5) is reported to regulate cell proliferation, apoptosis, and differentiation. Our study demonstrated a significant elevation of CCN5 expression in the testis of nonobstructive azoospermia patients and TM4 Sertoli cells exposed to BPA. Knockdown of CCN5 reduced apoptotic cells after BPA treatment, as determined by flow cytometry and terminal deoxynucleotidyl transferase dUTP nick end labeling assays. Cells exposed to BPA showed increased expressions of Bax and cleaved poly(ADP-ribose) polymerase, decreased expression of Bcl-2, as well as elevated activities of caspase-3 and caspase-9 in BPA-induced TM4 cells, which were reversed by CCN5 inhibition. Loss of CCN5 declined phosphorylation of protein kinase R-like endoplasmic reticulum kinase and eukaryotic translation initiation factor 2A and decreased activating transcription factor 4 and C/EBP-homologous protein in BPA-treated cells. Furthermore, silencing CCN5 blocked BPA-induced phosphorylation of p38 and c-Jun N-terminal kinase (JNK). Administration of anisomycin, a mitogen-activated protein kinase (MAPK) activator, reversed the effects of CCN5 knockdown on BPA-induced endoplasmic reticulum (ER) stress and apoptosis. Taken together, CCN5 promotes apoptosis and ER stress in Sertoli cells exposed to BPA by activating the p38/JNK MAPK signaling pathway.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"44 4","pages":"174-185"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143784646","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Role of microRNAs in Lidocaine-Induced Spinal Cord Neurotoxicity: An Exploration Based on Bioinformatics Analysis.

DNA and cell biology Pub Date : 2025-04-01 Epub Date: 2025-02-27 DOI: 10.1089/dna.2024.0215

Longyan Li, Zhong Zhang, Zhengwen Jia, Aimeng Tang, Qian Li

{"title":"The Role of microRNAs in Lidocaine-Induced Spinal Cord Neurotoxicity: An Exploration Based on Bioinformatics Analysis.","authors":"Longyan Li, Zhong Zhang, Zhengwen Jia, Aimeng Tang, Qian Li","doi":"10.1089/dna.2024.0215","DOIUrl":"10.1089/dna.2024.0215","url":null,"abstract":"This study investigated the impact of lidocaine-induced neurotoxicity on microRNA (miRNA) expression in the spinal cord of rats. Sprague-Dawley rats underwent intrathecal catheterization and were randomly assigned to receive either 10% lidocaine or normal saline for three consecutive days. Post-treatment, the paw withdrawal threshold significantly increased, accompanied by notable histopathological changes. Additionally, 470 miRNAs exhibited altered expression following lidocaine treatment, with miR-155-5p, miR-3544, and miR-675-5p showing significant changes. Gene Ontology analysis identified cellular metabolic processes as the most significantly enriched functions. Kyoto encyclopedia of genes and genomes pathway analysis revealed that the enriched signaling pathways are associated with neural injury and neuroprotection, and are involved in regulating cellular metabolism. The Mitogen-Activated Protein Kinase (MAPK) signaling pathway was notably enriched, with Mitogen-activated protein kinase kinase kinase 10 (Map3k10) and Mitogen-activated protein kinase kinase kinase 14 (Map3k14) identified as target genes of miR-155-5p. Following lidocaine treatment, there was an observed increase in the expression of MAP3K10 and MAP3K14 at both the mRNA and protein levels. These results indicate that miR-155-5p, miR-3544, and miR-675-5p might be significantly involved in lidocaine-induced neurotoxicity by influencing cellular metabolism. Furthermore, miR-155-5p/MAPK shows potential therapeutic value for treating lidocaine-induced neurotoxicity.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"186-196"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rosalind Franklin Society Proudly Announces the 2024 Award Recipient for DNA and Cell Biology.

DNA and cell biology Pub Date : 2025-04-01 DOI: 10.1089/dna.2024.0134.rfs2024

Sabrina Nolan Kline

引用次数: 0

Mechanism of LncRNA-MiRNA in Renal Intrinsic Cells of Diabetic Kidney Disease and Potential Therapeutic Direction. 糖尿病肾病肾固有细胞中 LncRNA-MiRNA 的作用机制及潜在治疗方向

DNA and cell biology Pub Date : 2025-03-21 DOI: 10.1089/dna.2025.0026

Xiyue Tian, Min Zhou, Jingbo Zhang, Xinchun Huang, Dongyang Jiang, Jian Liu, Qiong Zhang, Dingguo Chen, Qiongdan Hu

{"title":"Mechanism of LncRNA-MiRNA in Renal Intrinsic Cells of Diabetic Kidney Disease and Potential Therapeutic Direction.","authors":"Xiyue Tian, Min Zhou, Jingbo Zhang, Xinchun Huang, Dongyang Jiang, Jian Liu, Qiong Zhang, Dingguo Chen, Qiongdan Hu","doi":"10.1089/dna.2025.0026","DOIUrl":"https://doi.org/10.1089/dna.2025.0026","url":null,"abstract":"The occurrence of diabetic kidney disease (DKD), a critical microvascular issue in diabetes, is progressively on the rise. In recent years, long noncoding RNAs (lncRNAs) have garnered considerable attention as a novel and critical layer of biological regulation. Our knowledge regarding the roles and underlying mechanisms of lncRNAs in various diseases, including DKD, continues to evolve. Similarly, microRNAs (miRNAs), which are small noncoding RNAs, have been recognized as crucial contributors to cellular processes and disease pathogenesis. Emerging studies have highlighted the complex interactions between lncRNAs and miRNAs, particularly in the context of DKD, underscoring their importance in complex human diseases. Renal intrinsic cell damage is an important cause of inducing DKD. Persistent high glucose stimulation leads to remodeling of renal intrinsic cells and a cascade of pathological changes. This article aims to review recent literature on the lncRNAs-mediated regulation of miRNAs affecting renal intrinsic cells in DKD and to propose novel molecular-level therapeutic strategies for DKD. Through in-depth investigation of this dynamic molecular interaction, we can gain a profound understanding of the potential mechanisms underlying diabetic nephropathy, potentially identifying new targets for therapeutic intervention and paving the way for personalized and effective treatments.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143675119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Crosstalk Between Plk1 and PTEN in Mitosis Affects Chromosomal Stability.

DNA and cell biology Pub Date : 2025-03-21 DOI: 10.1089/dna.2024.0246

Wei Li, Xianning Wang, Jiannan Liu, Bing Liu, Yongjian Hao

{"title":"Crosstalk Between Plk1 and PTEN in Mitosis Affects Chromosomal Stability.","authors":"Wei Li, Xianning Wang, Jiannan Liu, Bing Liu, Yongjian Hao","doi":"10.1089/dna.2024.0246","DOIUrl":"https://doi.org/10.1089/dna.2024.0246","url":null,"abstract":"The mitotic phase involves the distribution and regulation of genetic material. Defects in gene regulation can lead to serious errors in genetic transmission, such as increased instability of chromosomes, thereby increasing susceptibility to cancer and promoting its development. The maintenance of chromosome stability depends on several mechanisms, such as efficient DNA repair, proper sister chromatid separation, and timely cytokinesis. The serine/threonine kinase Plk1 is a key molecule in maintaining chromosome stability, participating in multiple stages of precise regulation during mitosis, including promoting entry into mitosis, facilitating centrosome maturation and bipolar spindle formation, promoting sister chromatid separation, and facilitating cytokinesis. Several proteins can regulate the kinase activity of Plk1 through protein-protein interactions, coordinating the genetic stability of the cell, including the kinases Aurora A, c-Abl, and Chk1 as well as the phosphatase phosphatase and tension homolog (PTEN). PTEN has been described as an essential regulator of Plk1 for dephosphorylation and chromosomal stability during cell division, and Plk1 may directly interact with and phosphorylate PTEN at centromeres. Here, we review the bidirectional interplay between Plk1 and PTEN and how it contributes to genomic stability during mitosis.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143675056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Guardians of the Lung: The Multifaceted Roles of Macrophages in Cancer and Infectious Disease.

DNA and cell biology Pub Date : 2025-03-19 DOI: 10.1089/dna.2024.0211

Zhi Liu, Yangjing Ou, Xiaojin He, Ting Yuan, Miao Li, Yunzhu Long, Yukun Li, Yingzheng Tan

{"title":"Guardians of the Lung: The Multifaceted Roles of Macrophages in Cancer and Infectious Disease.","authors":"Zhi Liu, Yangjing Ou, Xiaojin He, Ting Yuan, Miao Li, Yunzhu Long, Yukun Li, Yingzheng Tan","doi":"10.1089/dna.2024.0211","DOIUrl":"https://doi.org/10.1089/dna.2024.0211","url":null,"abstract":"The lung as an organ that is fully exposed to the external environment for extended periods, comes into contact with numerous inhaled microorganisms. Lung macrophages are crucial for maintaining lung immunity and operate primarily through signaling pathways such as toll-like receptor 4 and nuclear factor-κB pathways. These macrophages constitute a diverse population with significant plasticity, exhibiting different phenotypes and functions on the basis of their origin, tissue residence, and environmental factors. During lung homeostasis, they are involved in the clearance of inhaled particles, cellular remnants, and even participate in metabolic processes. In disease states, lung macrophages transition from the inflammatory M1 phenotype to the anti-inflammatory M2 phenotype. These distinct phenotypes have varying transcriptional profiles and serve different functions, from combating pathogens to repairing inflammation-induced damage. However, macrophages can also exacerbate lung injury during prolonged inflammation or exposure to antigens. In this review, we delve into the diverse roles of pulmonary macrophages the realms in homeostasis, pneumonia, tuberculosis, and lung tumors.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665443","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Vitamin B12 in Cell Plasticity and Repair.

DNA and cell biology Pub Date : 2025-03-19 DOI: 10.1089/dna.2025.0037

Christina Fissoun, Marta Kovatcheva

引用次数: 0

VIRMA-Mediated the m6A Methylation of SCD Facilitates Wilms' Tumor Progression via AMPK Pathway.

DNA and cell biology Pub Date : 2025-03-05 DOI: 10.1089/dna.2024.0288

Songbai Zhu, Zhen Li

{"title":"VIRMA-Mediated the m6A Methylation of SCD Facilitates Wilms' Tumor Progression via AMPK Pathway.","authors":"Songbai Zhu, Zhen Li","doi":"10.1089/dna.2024.0288","DOIUrl":"https://doi.org/10.1089/dna.2024.0288","url":null,"abstract":"Wilms' tumor (WT) is the most prevalent renal cancer in children. Numerous studies have shown that vir-like n6-methyladenosine (m6A) methyltransferase-associated protein (VIRMA), a necessary component and the largest methyltransferase, contributes to the advancement of multiple cancers. However, its function has not been characterized in WT. Hence, we examined the potential role of VIRMA in WT by analyzing its effect on the m6A modification of stearoyl-CoA desaturase (SCD). We utilized bioinformatics to narrow 12 differentially expressed (DE) genes in WT to a single gene. The expressions of SCD and VIRMA were analyzed via quantitative real-time PCR and western blotting. The influence of SCD on the malignancy attributes of WT cells and adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling was assessed through Cell counting Kit-8, Ethynyl-2'-deoxyuridine, transwell, and western blotting assays. The specific interactions between SCD and VIRMA were confirmed through methylated RNA immunoprecipitation, western blotting, and RNA stability assays, followed by rescue experiments to show underlying mechanisms. The SCD expression was found to be elevated in WT samples. Furthermore, its silencing mitigated the malignant characteristics of WT cells while increasing the protein levels of key AMPK signaling molecules. Moreover, VIRMA was also upregulated in WT samples and demonstrated a positive association with SCD expression. The relative enrichment of SCD m6A, its protein, and its mRNA stability were enhanced in VIRMA-overexpressed WT cells. Mechanically, VIRMA overexpression accelerated the malignant phenotypes of WT cells by interacting with SCD. Overall, the results demonstrate that VIRMA-mediated m6A methylation of SCD promotes WT progression by modulating the AMPK pathway.","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143560304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0