ArticleJournal of the National Cancer Center2021
Chromatin assembly factor 1 suppresses epigenetic reprogramming toward adaptive drug resistance.
Article in Journal of the National Cancer Center, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Aberrant heterochromatin silences immune response genes in chronic lymphocytic leukemia.Blood neoplasia · 2025Article
- Current understanding of epigenetics role in melanoma treatment and resistance.Cancer cell international · 2022Review
- Chemotherapy-induced nephrotoxicity was improved by crocin in mouse model.European journal of histochemistry : EJH · 2022Article
- B cell receptor signaling drives APOBEC3 expression via direct enhancer regulation in chronic lymphocytic leukemia B cells.Blood cancer journal · 2022Article
- High expression of H2A histone family member Y promotes the proliferation and autophagy of hepatocellular carcinoma cells.Bioengineered · 2022Article
- Oncolytic Adenovirus with SPAG9 shRNA Driven by DD3 Promoter Improved the Efficacy of Docetaxil for Prostate Cancer.Journal of oncology · 2022Article
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Authors and funding
6 authors.
Funding
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Abstract
The long-term effectiveness of targeted cancer therapies is limited by the development of resistance. Although epigenetic reprogramming has been implicated in resistance, the mechanisms remain elusive. Herein, we demonstrate that increased chromatin accessibility is involved in adaptive BRAF inhibitor (BRAFi)-resistance in melanoma cells. We observed loss of chromatin assembly factor 1 (CAF-1) and its related histone H3 lysine 9 trimethylation (H3K9me3) with adaptive BRAFi resistance. We further showed that depletion of CAF-1 provides chromatin plasticity for effective reprogramming by AP1 components to promote BRAFi resistance. Our data suggest that therapeutic approaches to restore H3K9me3 levels may compensate for the loss of CAF-1 and, in turn, suppress resistance to BRAF inhibitors.
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