ArticleThe Kaohsiung journal of medical sciences2020
Chidamide acts on the histone deacetylase-mediated miR-34a/Bcl-2 axis to regulate NB4 cell line proliferation and apoptosis.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Immune escape mechanisms and therapeutic advances in virus-associated hematological malignancies.Blood cancer journal · 2026Review
- Epigenetic remodeling and apoptotic activation by Chidamide suppress small cell lung cancer in molecularly distinct subtypes.Discover oncology · 2026Article
- HBx hijacks the miR-19a-3p/BAMBI/TGF-β1 axis to impair the anti-tumour activity of CD4Clinical and translational medicine · 2026Article
- Molecular mechanisms of viral oncogenesis in haematological malignancies: perspectives from metabolic reprogramming, epigenetic regulation and immune microenvironment remodeling.Experimental hematology & oncology · 2025Review
- Chidamide and venetoclax synergistically regulate the Wnt/β-catenin pathway by MYCN/DKK3 in B-ALL.Annals of hematology · 2025Article
- Chidamide works synergistically with Dasatinib by inducing cell-cycle arrest and apoptosis in acute myeloid leukemia cells.Molecular and cellular biochemistry · 2023Article
- HBV-associated DLBCL of poor prognosis: advance in pathogenesis, immunity and therapy.Frontiers in immunology · 2023Review
- Chidamide acts on the histone deacetylase-mediated miR-34a/Bcl-2 axis to regulate NB4 cell line proliferation and apoptosis.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute promyelocytic leukemia (APL), a biologically and clinically distinct variant of acute myelogenous leukemia, is characterized by the fusion of the N-terminus of promyelocytic leukemia protein to the C terminus of retinoic acid receptor alpha, mostly due to chromosomal translocation t(15;17). Chidamide, a synthetic analogue of MS-275 identified from a group of benzamide-type compounds, has been found to have efficient anticancer activity in basic and clinical research studies. However, the concrete role and underlying mechanism of Chidamide in the treatment of APL has not been well characterized. Our data demonstrate that Chidamide inhibited the expression of histone deacetylase (HDAC) to induce apoptosis and suppress proliferation in NB4 cells. Mechanistically, Chidamide increases the expression of miR-34a by suppressing HDAC. Furthermore, B-cell lymphoma-2 (Bcl-2) is a direct target of miR-34a, the expression of which is regulated by miR-34a. Functionally, Chidamide inhibits cell proliferation and promotes apoptosis through miR-34a/Bcl-2. Chidamide exerts its anticancer effect via the HDAC-mediated miR-34a/Bcl-2 axis, providing potential targets for APL therapy.
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