RNA-DNA hybridization in a solution with DNA excess was employed. Rat's livers were given one injection of 4-dimethylaminoazobenzene, and, when compared 24 hours afterwards with livers from normal untreated rats, demonstrated an altered transcription. The hybridization capacity of the nuclear RNA isolated from carcinogen-treated livers is lower than that of the control RNA. The changes observed in the carcinogen treated RNA population may be due to changes in the rate of transcription in DNA sites.
Download full-text PDF |
Source |
|---|
Publication Analysis
Top Keywords
Similar Publications
Polydatin protects against DSS-induced ulcerative colitis via Nrf2/Slc7a11/Gpx4-dependent inhibition of ferroptosis signalling activation.
Front Pharmacol
January 2025
Department of Gastroenterology, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
Introduction: Ulcerative colitis (UC), a form of inflammatory irritable bowel disease, is characterized by a recurrent and persistent nonspecific inflammatory response. Polydatin (PD), a natural stilbenoid polyphenol with potent properties, exhibits unexpected beneficial effects beyond its well-documented anti-inflammatory and antioxidant activities. In this study, we presented evidence that PD confers protection against dextran sodium sulfate (DSS)-induced ulcerative colitis.
View Article and Find Full Text PDFSpecific modulation of 28S_Um2402 rRNA 2'--ribose methylation as a novel epitranscriptomic marker of ZEB1-induced epithelial-mesenchymal transition in different mammary cell contexts.
NAR Cancer
March 2025
Ribosome, Translation and Cancer Team, LaEx DEVweCAN, Institut Convergence Plascan, LYriCAN+, Centre de Recherche en Cancérologie de Lyon, INSERM U1052, CNRS UMR 5286, Centre Léon Bérard, Université de Lyon, Université Claude Bernard Lyon 1, 69008 Lyon, France.
The epithelial-mesenchymal transition (EMT) is a dynamic transdifferentiation of epithelial cells into mesenchymal cells. EMT programs exhibit great diversity, based primarily on the distinct impact of molecular activities of the EMT transcription factors. Using a panel of cancer cell lines and a series of 71 triple-negative primary breast tumors, we report that the EMT transcription factor ZEB1 modulates site-specific chemical modifications of ribosomal RNA (rRNA).
View Article and Find Full Text PDFMolecular and functional profiling unravels targetable vulnerabilities in colorectal cancer.
Mol Oncol
January 2025
Division of Molecular Genome Analysis, German Cancer Research Center, Heidelberg, Germany.
Colorectal cancer (CRC) patients with microsatellite-stable (MSS) tumors are mostly treated with chemotherapy. Clinical benefits of targeted therapies depend on mutational states and tumor location. Many tumors carry mutations in KRAS proto-oncogene, GTPase (KRAS) or B-Raf proto-oncogene, serine/threonine kinase (BRAF), rendering them more resistant to therapies.
View Article and Find Full Text PDFNEAT1 regulates BMSCs aging through disruption of FGF2 nuclear transport.
Stem Cell Res Ther
January 2025
College & Hospital of Stomatology, Key Laboratory of Oral Diseases Research of Anhui Province, Anhui Medical University, Hefei, 230032, China.
Background: The aging of bone marrow mesenchymal stem cells (BMSCs) impairs bone tissue regeneration, contributing to skeletal disorders. LncRNA NEAT1 is considered as a proliferative inhibitory role during cellular senescence, but the relevant mechanisms remain insufficient. This study aims to elucidate how NEAT1 regulates mitotic proteins during BMSCs aging.
View Article and Find Full Text PDFCXCR4 promotes tumor stemness maintenance and CDK4/6 inhibitors resistance in ER-positive breast cancer.
Breast Cancer Res
January 2025
Guangdong Provincial Key Laboratory of Malignant Tumor Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, 510120, China.
Background: CDK4/6 inhibitors have significantly improved the survival of patients with HR-positive/HER2-negative breast cancer, becoming a first-line treatment option. However, the development of resistance to these inhibitors is inevitable. To address this challenge, novel strategies are required to overcome resistance, necessitating a deeper understanding of its mechanisms.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!