Open AccessChidamide suppresses the glycolysis of triple negative breast cancer cells partially by targeting the miR‑33a‑5p‑LDHA axis
Author(s) -
Xuejuan Bai,
Hongchuan Jiang,
Guohui Han,
Qiang He
Publication year - 2019
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2019.10425
Subject(s) - triple negative breast cancer , lactate dehydrogenase a , cancer research , biology , oncogene , cancer , microrna , breast cancer , cell cycle , glycolysis , chemistry , endocrinology , biochemistry , metabolism , gene , genetics
Triple negative breast cancer (TNBC) is one of the most aggressive types of breast cancer and has a poor prognosis. Therefore, the development of novel drugs and understanding the molecular mechanisms that may contribute to the initiation and development of TNBC are urgently required. Chidamide, a histone deacetylase inhibitor, has been reported as possessing anti‑cancer properties in several cancers, however, the function of chidamide in TNBC remains to be elucidated. The present study revealed that chidamide inhibited the proliferation, colony formation and migration of TNBC cells. Experiments investigating the underlying mechanism revealed that chidamide upregulated the expression of microRNA (miR)‑33a‑5p in TNBC cells via RT‑qPCR. Luciferase reporter assay demonstrated that miR‑33a‑5p was bound to the 3'‑untranslated region of lactate dehydrogenase A (LDHA) and decreased the expression of LDHA in TNBC cells. In addition, chidamide suppressed the expression of LDHA and significantly decreased the glycolysis of TNBC cells. Collectively, the results of the present study demonstrated that chidamide reprogramed glucose metabolism, partially by targeting the miR‑33a‑5p/LDHA pathway, in TNBC. These findings indicate that chidamide may be a promising novel drug in the treatment of patients with TNBC.