The integrity of the genetic material in human cells is continuously challenged by environmental agents and endogenous stresses. Among these, environmental carcinogens are pivotal in initiating complex DNA lesions that can lead to malignant transformations if not properly repaired. This review synthesizes current knowledge on the molecular dynamics of DNA repair mechanisms and their interplay with various environmental carcinogens, providing a comprehensive overview of how these interactions contribute to cancer initiation and progression. We examine key DNA repair pathways including base excision repair, nucleotide excision repair, and double-strand break repair and their regulatory networks, highlighting how defects in these pathways can exacerbate carcinogen-induced damage. Further, we discuss how understanding these molecular interactions offers novel insights into potential therapeutic strategies. This includes leveraging synthetic lethality concepts and designing targeted therapies that exploit specific DNA repair vulnerabilities in cancer cells. By integrating recent advances in molecular biology, genetics, and oncology, this review aims to illuminate the complex landscape of DNA repair and carcinogen-induced carcinogenesis, setting the stage for future research and therapeutic innovations.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.mrfmmm.2024.111883 | DOI Listing |
Methods Mol Biol
January 2025
Stem Cell Program, Boston Children's Hospital, Boston, MA, USA.
The CRISPR-activated repair lineage tracing (CARLIN) mouse line uses DNA barcoding to enable high-resolution tracing of cell lineages in vivo (Bowling et al, Cell 181, 1410-1422.e27, 2020). CARLIN mice contain expressed barcodes that allow simultaneous interrogation of lineage and gene expression information from single cells.
View Article and Find Full Text PDFAppl Environ Microbiol
December 2024
School of Medicine, Nankai University, Tianjin, Tianjin, China.
is a foodborne pathogen linked to severe infections in infants and often associated with contaminated powdered infant formula. The RecA protein, a key player in DNA repair and recombination, also influences bacterial resilience and virulence. This study investigated the impact of deletion on the pathogenicity and environmental stress tolerance of BAA-894.
View Article and Find Full Text PDFJ Med Chem
January 2025
SANKEN, Osaka University, Mihogaoka, Ibaraki-shi, Osaka 567-0047, Japan.
Histone methylation, a crucial aspect of epigenetics, intricately involves specialized enzymes such as G9a, a histone methyltransferase (HMT) catalyzing the methylation of histone H3 lysine 9 (H3K9) and H3K27. Apart from histone modification, G9a regulates essential cellular processes such as deoxyribonucleic acid (DNA) replication, damage repair, and gene expression via modulating DNA methylation patterns. The dysregulation and overexpression of G9a are intricately linked to cancer initiation, progression, and metastasis, making it a compelling target for anticancer therapy.
View Article and Find Full Text PDFBiosci Rep
January 2025
Tata Institute of Fundamental Research, Bangalore, India.
The tumor suppressor PALB2 is a key player in the Homologous Recombination (HR) pathway, functionally connecting BRCA proteins at the DNA damage site. PALB2 forms homodimers via its coiled-coil domain, and during HR, it forms a heterodimeric complex with BRCA1 using the same domain. However, the structural details of the human PALB2 coiled-coil domain are unknown.
View Article and Find Full Text PDFInt J Med Sci
January 2025
Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
Growing research suggests that endometriosis and systemic lupus erythematosus (SLE) are both chronic inflammatory diseases and closely related, but no studies have explored their common molecular characteristics and underlying mechanisms. Based on GEO datasets, differentially expressed genes in the endometriosis cohort and the SLE cohort were screened using Limma and weighted gene co-expression network analysis (WGCNA), and prediction signatures were constructed using LASSO logistic regression analysis, respectively. Four co-diagnostic genes (PMP22, QSOX1, REV3L, SP110) were identified for endometriosis and SLE.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!