PUBLICATIONS
Transcription factors, nucleotide excision repair, and cancer: A review of molecular interplay
Bulky DNA adducts are mostly formed by external factors such as UV irradiation, smoking or treatment with DNA crosslinking agents. If such DNA adducts are not removed by nucleotide excision repair, they can lead to formation of driver mutations that contribute to cancer formation. Transcription factors (TFs) may critically affect both DNA adduct formation and repair efficiency at the binding site to DNA. For example, “hotspot” mutations in melanoma coincide with UV-induced accumulated cyclobutane pyrimidine dimer (CPD) adducts and/or inhibited repair at the binding sites of some TFs. Similarly, anticancer treatment with DNA cross-linkers may additionally generate DNA adducts leading to secondary mutations and the formation of malignant subclones. In addition, some TFs are overexpressed in response to UV irradiation or chemotherapeutic treatment, activating oncogenic and anti-oncogenic pathways independently of nucleotide excision repair itself. This review focuses on the interplay between TFs and nucleotide excision repair during cancer development and progression.
- Related:
- Genome-wide strand-specific UV mutagenesis in Escherichia coli is directed by the Mfd translocase
- Chromatin context shapes DNA damage formation and nucleotide excision repair dynamics in Caenorhabditis elegans
- UV-induced reorganization of 3D genome mediates DNA damage response
- Dynamics of transcription-coupled repair of cyclobutane pyrimidine dimers and (6-4) photoproducts in Escherichia coli
- Global repair is the primary nucleotide excision repair subpathway for the removal of pyrimidine-pyrimidone (6-4) damage from the Arabidopsis genome
- The interplay of 3D genome organization with UV-induced DNA damage and repair
- The Mfd protein is the Transcription-Repair Coupling Factor (TRCF) in Mycobacterium smegmatis
- Effects of replication domains on genome-wide UV-induced DNA damage and repair
- Genome-wide Excision Repair Map of Cyclobutane Pyrimidine Dimers in Arabidopsis and the Roles of CSA1 and CSA2 Proteins in Transcription-Coupled Repair
- CSB-independent, XPC-dependent transcription-coupled repair in Drosophila.
- Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events
- Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells
- Differential damage and repair of anti-cancer drug cisplatin induced DNA-adducts across mouse organs
- Genome-wide mapping of nucleotide excision repair with XR-seq.
- Cisplatin-DNA adduct repair of transcribed genes is controlled by two circadian programs in mouse tissues.
- Genome-wide Excision Repair in Arabidopsis is coupled to transcription and reflects circadian gene expression patterns.
- Single-nucleotide resolution dynamic repair maps of UV damage in Saccharomyces cerevisiae genome.
- Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli.
- Molecular mechanism of DNA excision repair and excision repair maps of the human and E. coli genomes.
- Dynamic maps of UV damage formation and repair.
- Human genome-wide repair map of DNA damage caused by the cigarette smoke carcinogen benzo[a]pyrene.
- Genome-wide transcription-coupled repair in Escherichia coli is mediated by the Mfd translocase.