ArticleMolecular cancer research : MCR2015
c-MYC Generates Repair Errors via Increased Transcription of Alternative-NHEJ Factors, LIG3 and PARP1, in Tyrosine Kinase-Activated Leukemias.
Article in Molecular cancer research : MCR, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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45 citing papers in PubMed, 66 citations in OpenAlex.
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- Knockdown of ASF1B inhibits cell proliferation, migration, invasion and cisplatin resistance in gastric cancer through the Myc pathway.Oncology letters · 2023Article
- Exploiting DNA Ligase III addiction of multiple myeloma by flavonoid Rhamnetin.Journal of translational medicine · 2022Article
- Activating STING1-dependent immune signaling inProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Role of EMT in the DNA damage response, double-strand break repair pathway choice and its implications in cancer treatment.Cancer science · 2022Review
- Implication of microRNAs in Carcinogenesis with Emphasis on Hematological Malignancies and Clinical Translation.International journal of molecular sciences · 2022Review
- Chromosomal Instability in Chronic Myeloid Leukemia: Mechanistic Insights and Effects.Cancers · 2022Review
- Therapeutic Targeting of FLT3 in Acute Myeloid Leukemia: Current Status and Novel Approaches.OncoTargets and therapy · 2022Review
- Roles of miRNA dysregulation in the pathogenesis of multiple myeloma.Cancer gene therapy · 2021Review
- PARP1 as a therapeutic target in acute myeloid leukemia and myelodysplastic syndrome.Blood advances · 2021Review
- Involvement of classic and alternative non-homologous end joining pathways in hematologic malignancies: targeting strategies for treatment.Experimental hematology & oncology · 2021Review
- Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
unlabelledLeukemias expressing the constitutively activated tyrosine kinases (TK) BCR-ABL1 and FLT3/ITD activate signaling pathways that increase genomic instability through generation of reactive oxygen species (ROS), DNA double-strand breaks (DSB), and error-prone repair. The nonhomologous end-joining (NHEJ) pathway is a major pathway for DSB repair and is highly aberrant in TK-activated leukemias; an alternative form of NHEJ (ALT-NHEJ) predominates, evidenced by increased expression of DNA ligase IIIα (LIG3) and PARP1, increased frequency of large genomic deletions, and repair using DNA sequence microhomologies. This study, for the first time, demonstrates that the TK target c-MYC plays a role in transcriptional activation and subsequent expression of LIG3 and PARP1 and contributes to the increased error-prone repair observed in TK-activated leukemias. c-MYC negatively regulates microRNAs miR-150 and miR-22, which demonstrate an inverse correlation with LIG3 and PARP1 expression in primary and cultured leukemia cells and chronic myelogenous leukemia human patient samples. Notably, inhibition of c-MYC and overexpression of miR-150 and -22 decreases ALT-NHEJ activity. Thus, BCR-ABL1 or FLT3/ITD induces c-MYC expression, leading to genomic instability via augmented expression of ALT-NHEJ repair factors that generate repair errors. IMPLICATIONS: In the context of TK-activated leukemias, c-MYC contributes to aberrant DNA repair through downstream targets LIG3 and PARP1, which represent viable and attractive therapeutic targets.
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