ArticleThe Journal of biological chemistry2010
Anti-apoptotic protein BCL2 down-regulates DNA end joining in cancer cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed.
- Caffeine inhibits nonhomologous end joining by impairing ligase IV/XRCC4 function.Nucleic acids research · 2026Article
- Homoharringtonine enhances cytarabine-induced apoptosis in acute myeloid leukaemia by regulating the p38 MAPK/H2AX/Mcl-1 axis.BMC cancer · 2024Article
- Therapeutic targeting of nuclear export and import receptors in cancer and their potential in combination chemotherapy.IUBMB life · 2024Review
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- Article
- Nonamer dependent RAG cleavage at CpGs can explain mechanism of chromosomal translocations associated to lymphoid cancers.PLoS genetics · 2022Article
- Venetoclax enhances DNA damage induced by XPO1 inhibitors: A novel mechanism underlying the synergistic antileukaemic effect in acute myeloid leukaemia.Journal of cellular and molecular medicine · 2022Article
- Structural Details of BH3 Motifs and BH3-Mediated Interactions: an Updated Perspective.Frontiers in molecular biosciences · 2022Review
- Characterization of G-quadruplex antibody reveals differential specificity for G4 DNA forms.DNA research : an international journal for rapid publication of reports on genes and genomes · 2020Article
- BCL-2 family isoforms in apoptosis and cancer.Cell death & disease · 2019Review
- Homologous recombination-mediated repair of DNA double-strand breaks operates in mammalian mitochondria.Cellular and molecular life sciences : CMLS · 2018Article
- DNA double-strand break repair in Penaeus monodon is predominantly dependent on homologous recombination.DNA research : an international journal for rapid publication of reports on genes and genomes · 2017Article
- Microhomology-mediated end joining is the principal mediator of double-strand break repair during mitochondrial DNA lesions.Molecular biology of the cell · 2016Article
- Homology and enzymatic requirements of microhomology-dependent alternative end joining.Cell death & disease · 2015Article
- Obatoclax potentiates the cytotoxic effect of cytarabine on acute myeloid leukemia cells by enhancing DNA damage.Molecular oncology · 2015Article
- Exploiting base excision repair to improve therapeutic approaches for pancreatic cancer.Frontiers in nutrition · 2015Review
- Inhibition of PARP1-dependent end-joining contributes to Olaparib-mediated radiosensitization in tumor cells.Molecular oncology · 2014Article
- G-quadruplex structures formed at the HOX11 breakpoint region contribute to its fragility during t(10;14) translocation in T-cell leukemia.Molecular and cellular biology · 2013Article
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- Mechanism of fragility at BCL2 gene minor breakpoint cluster region during t(14;18) chromosomal translocation.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer cells are often associated with secondary chromosomal rearrangements, such as deletions, inversions, and translocations, which could be the consequence of unrepaired/misrepaired DNA double strand breaks (DSBs). Nonhomologous DNA end joining is one of the most common pathways to repair DSBs in higher eukaryotes. By using oligomeric DNA substrates mimicking various endogenous DSBs in a cell-free system, we studied end joining (EJ) in different cancer cell lines. We found that the efficiency of EJ varies among cancer cells; however, there was no remarkable difference in the mechanism and expression of EJ proteins. Interestingly, cancer cells with lower levels of EJ possessed elevated expression of BCL2 and vice versa. Removal of BCL2 by immunoprecipitation or protein fractionation led to elevated EJ. More importantly, we show that overexpression of BCL2 or the addition of purified BCL2 led to the down-regulation of EJ. Further, we found that BCL2 interacts with KU proteins both in vitro and in vivo. Hence, our results suggest that EJ in cancer cells could be negatively regulated by the anti-apoptotic protein, BCL2, and this may contribute toward increased chromosomal abnormalities in cancer.
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