DNA and cell biology最新文献

{"title":"Therapeutic Efficacy of Melatonin and Flutamide Combination in Safety for Prostate Cancer: An <i>In Vitro</i> Study.","authors":"Reza Omid, Fatemeh Khatami, Ramin Rahimnia, Diana Taheri, Rahil Mashhadi, Akram Mirzaei, Seyedeh Fatemeh Hosseini, Seyedeh Negin Hashemi Dougaheh, Leonardo Oliveira Reis, Seyed Mohammad Kazem Aghamir","doi":"10.1089/dna.2025.0018","DOIUrl":"10.1089/dna.2025.0018","url":null,"abstract":"<p><p>The side effects associated with flutamide as a first-line drug treating prostate cancer, including hepatotoxicity, the aim of this research was to use melatonin as an anticancer candidate to reduce the dose of flutamide and reduce its side effects. We evaluated the effect of melatonin, flutamide, and melatonin-flutamide combination therapy in LNCaP, DU145, and PC3 cell lines. The assessment includes Hoechst dye staining, scratch-wound assay, colony formation assay, flow cytometric analysis of apoptosis and DNA cell cycle, real-time PCR (<i>BAX [BCL2 Associated X]/B-cell lymphoma-2 [BCL2]</i>, <i>E-cadherin</i>, Zinc finger protein SNAI2 [<i>SNAIL]</i>, Hypoxia Inducible Factor 1 Subunit Alpha [<i>HIF1α]</i>, Vascular Endothelial Growth Factor C [<i>VEGFC]</i>, and <i>kallikrein-related peptidase 3</i> [<i>KLK3</i>] genes). To determine Half maximal inhibitory concentration (IC50) levels, cell lines were exposed to different concentrations of the drugs. Our data indicated that IC50 values for melatonin (75 µM) and three cell lines and flutamide (12 and 10 µM) for PC3 and LNCaP/DU145, respectively, with 3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyl tetrazolium bromide were approved by flow cytometry in a dose and time-dependent manner which was as a consequence of cell cycle arrest at G0/G1 phase. Due to the efficacy of melatonin in combination with flutamide, we used 75 µM melatonin, and 5 µM flutamide instead of 12 µM in DU145, and 6 µM in PC3 and LNCaP, respectively. The combination of melatonin and flutamide significantly upregulated the expression of <i>BAX/BCL2</i> ratio in all three cell lines (<i>p</i> < 0.0001) and downregulated the expression of <i>KLK3</i> (<i>p</i> < 0.01), <i>HIF1α</i> (<i>p</i> < 0.01), <i>VEGFC</i> (<i>p</i> < 0.001), and epithelial-mesenchymal transition pathway genes in PC3 and LNCaP (<i>p</i> < 0.01). Melatonin in combination with flutamide reduced its dose and increased the sensitivity of prostate cancer cells to treatment.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"325-337"},"PeriodicalIF":0.0,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144121794","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}

{"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":"10.1089/dna.2024.0280","url":null,"abstract":"<p><p>This study presents a case of autosomal dominant polycystic kidney disease (ADPKD) involving a mosaic microdeletion in the <i>PKD1</i> 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 <i>PKD1</i> gene because of the mosaic deletion mutation of <i>PKD1</i> 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.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"238-248"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","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}

{"title":"Vitamin B12 in Cell Plasticity and Repair.","authors":"Christina Fissoun, Marta Kovatcheva","doi":"10.1089/dna.2025.0037","DOIUrl":"10.1089/dna.2025.0037","url":null,"abstract":"<p><p>Cellular plasticity, which refers to the capacity of cells to alter their identity or potency in response to a variety of stimuli, is emerging as an essential component in tissue repair. Despite the fact that stem cells have historically been considered to be the major agents of plasticity, new research has demonstrated that even differentiated cells in organs including the stomach, pancreas, and lungs are capable of displaying plasticity under specific physiological conditions, such as during injury and repair. One element essential for many physiological processes is vitamin B12 (VB12). Beyond its well-known roles in red blood cell production and nervous system maintenance, VB12 is critical for one-carbon metabolism and DNA synthesis and repair, processes indispensable for cellular health and tissue integrity. With its wide spectrum of actions, VB12 may have the potential to significantly influence tissue plasticity and repair, paving the way for new therapeutic interventions. Investigating fundamental processes and considering consequences for illness and aging, this perspective contemplates the junction of VB12, cell plasticity, and tissue repair.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"209-213"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143665499","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}

{"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":"10.1089/dna.2024.0288","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":" ","pages":"229-237"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","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}

{"title":"Structural Dynamics, Evolutionary Significance, and Functions of Really Interesting New Gene Proteins in Ubiquitination and Plant Stress: A Review.","authors":"Parinita Agarwal, Anjali Chittora, Ayushi Verma, Pradeep K Agarwal","doi":"10.1089/dna.2025.0002","DOIUrl":"https://doi.org/10.1089/dna.2025.0002","url":null,"abstract":"<p><p>Abiotic stress causes major crop losses worldwide. Plants have evolved complex intricate signaling network involving transcriptional regulators and posttranslational modifications (PTMs). Ubiquitination-a key PTM-regulates protein degradation through the ubiquitin-proteasome system (UPS). The UPS plays a pivotal role in detecting and modulating plant responses to environmental fluctuations. The E3 ligase family in plants is extensive, offering high substrate specificity and playing a vital role in signaling and protein turnover. Really Interesting New Gene (RING) proteins primarily function as E3 ubiquitin ligases, their functional diversity facilitates the transfer of ubiquitin molecules to specific target proteins. Plants possess abscisic acid (ABA)-dependent and ABA-independent stress-signaling pathways. RING-type E3 ligases regulate ABA signaling either negatively or positively in response to stress by regulating protein degradation, modulating transcription factors, ABA biosynthesis, and degradation. This dynamic interaction between ABA and E3 ligase proteins helps plants to adapt to environmental stress. Negative regulators, such as AIP2 and OsDSG1, target ABI3 for degradation. Keep on going (KEG) ubiquitinates ABI5, ABF1, and ABF3, though KEG itself is subject to feedback regulation by ABA levels, leading to its degradation. Positive regulators include SDIR1, OsSDIR1, AIRP1, RHA2b/RHA2a, and XERICO, along with its maize orthologs ZmXerico1 and ZmXerico2. Additionally, SINAT5 and BOI regulate auxin and gibberellin signaling, integrating hormonal responses to stress. The functional diversity of RING-type E3 ligases offers promising targets for genetic engineering to enhance crop resilience under adverse environmental conditions. Understanding these molecular mechanisms could lead to the development of climate-resilient crops, crucial for sustaining global food security.</p>","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"44 5","pages":"214-228"},"PeriodicalIF":0.0,"publicationDate":"2025-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144052220","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}

{"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":"<p><p>Liquiritin, a key component extracted from <i>Glycyrrhiza radix</i>, 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 <i>in vivo</i>. 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.</p>","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}

{"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":"10.1089/dna.2024.0247","url":null,"abstract":"<p><p>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 <i>CCN5</i> 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 <i>CCN5</i> inhibition. Loss of <i>CCN5</i> 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 <i>CCN5</i> 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 <i>CCN5</i> 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.</p>","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}

{"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":"<p><p>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 <i>miR-155-5p</i>, <i>miR-3544</i>, and <i>miR-675-5p</i> 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 <i>Mitogen-activated protein kinase kinase kinase 10 (Map3k10)</i> and <i>Mitogen-activated protein kinase kinase kinase 14 (Map3k14)</i> identified as target genes of <i>miR-155-5p</i>. 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 <i>miR-155-5p</i>, <i>miR-3544</i>, and <i>miR-675-5p</i> might be significantly involved in lidocaine-induced neurotoxicity by influencing cellular metabolism. Furthermore, <i>miR-155-5p</i>/MAPK shows potential therapeutic value for treating lidocaine-induced neurotoxicity.</p>","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}

{"title":"Rosalind Franklin Society Proudly Announces the 2024 Award Recipient for <i>DNA and Cell Biology</i>.","authors":"Sabrina Nolan Kline","doi":"10.1089/dna.2024.0134.rfs2024","DOIUrl":"https://doi.org/10.1089/dna.2024.0134.rfs2024","url":null,"abstract":"","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"44 4","pages":"173"},"PeriodicalIF":0.0,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143784647","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}

{"title":"Acknowledgment of Reviewers 2024.","authors":"","doi":"10.1089/dna.2024.87510.revack","DOIUrl":"https://doi.org/10.1089/dna.2024.87510.revack","url":null,"abstract":"","PeriodicalId":93981,"journal":{"name":"DNA and cell biology","volume":"44 2","pages":"125-126"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143257434","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}