M.D., Taipei Medical University
Post Doctoral Fellowship, Kenneth R. Chien Lab, UCSD, U.S.A
Scope: This study investigated the effect of epigallocatechin gallate (EGCG) on white and beige preadipocyte growth and explored the involvement of the miR-let-7a/HMGA2 pathway.
Methods and results: 3T3-L1 and D12 cells were treated with EGCG. The effect of EGCG on cell proliferation and viability was evaluated, as well as microRNA (miRNA)-related signaling pathways. EGCG inhibited 3T3-L1 and D12 preadipocyte growth, upregulated miR-let-7a expression, and downregulated high-mobility group AT-hook 2 (HMGA2) mRNA and protein levels in a time- and dose-dependent manner. In addition, overexpression of miR-let-7a significantly inhibited the growth of 3T3-L1 and D12 cells and decreased HMGA2 mRNA and protein levels. MiR-let-7a inhibitor antagonized the inhibitory effects of EGCG on the number and viability of 3T3-L1 and D12 cells. Furthermore, miR-let-7a inhibitor reversed the EGCG-induced increase in miR-let-7a expression levels and decrease in HMGA2 mRNA and protein levels. HMGA2 overexpression induced an increase in cell number and viability and antagonized EGCG-suppressed cell growth and HMGA2 expression in 3T3-L1 and D12 preadipocytes.
Conclusion: EGCG inhibits the growth of 3T3-L1 and D12 preadipocytes by modulating the miR-let-7a and HMGA2 pathways. This article is protected by copyright. All rights reserved.