Chen Wen-Ting, Yang Meei-Ju, Tsuei Yi-Wei, Su Tsung-Chen, Siao An-Ci, Kuo Yow-Chii, Huang Ling-Ru, Chen Yi, Chen Sy-Jou, Chen Po-Chuan, Cheng Ching-Feng, Ku Hui-Chen, Kao Yung-Hsi
Department of Life Sciences, National Central University, Taoyuan, 320, Taiwan.
Tea Research and Extension Station, Council of Agriculture, Executive Yuan Number 324 Chung-Hsing RD., Taoyuan, 326, Taiwan.
Mol Nutr Food Res. 2023 May;67(9):e2200336. doi: 10.1002/mnfr.202200336. Epub 2023 Mar 20.
This study investigates the effect of epigallocatechin gallate (EGCG) on white and beige preadipocyte growth and explores the involvement of the miR-let-7a/HMGA2 pathway.
3T3-L1 and D12 cells are treated with EGCG. The effect of EGCG on cell proliferation and viability is evaluated, as well as microRNA (miRNA)-related signaling pathways. EGCG inhibits 3T3-L1 and D12 preadipocyte growth, upregulates miR-let-7a expression, and downregulates 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 inhibits the growth of 3T3-L1 and D12 cells and decreases HMGA2 mRNA and protein levels. MiR-let-7a inhibitor antagonizes the inhibitory effects of EGCG on the number and viability of 3T3-L1 and D12 cells. Furthermore, miR-let-7a inhibitor reverses the EGCG-induced increase in miR-let-7a expression levels and decrease in HMGA2 mRNA and protein levels. HMGA2 overexpression induces an increase in cell number and viability and antagonizes EGCG-suppressed cell growth and HMGA2 expression in 3T3-L1 and D12 preadipocytes.
EGCG inhibits the growth of 3T3-L1 and D12 preadipocytes by modulating the miR-let-7a and HMGA2 pathways.
本研究调查表没食子儿茶素没食子酸酯（EGCG）对白色和米色前脂肪细胞生长的影响，并探讨miR-let-7a/HMGA2通路的参与情况。
用EGCG处理3T3-L1和D12细胞。评估EGCG对细胞增殖和活力的影响以及与微小RNA（miRNA）相关的信号通路。EGCG以时间和剂量依赖性方式抑制3T3-L1和D12前脂肪细胞生长，上调miR-let-7a表达，并下调高迁移率族AT钩蛋白2（HMGA2）的mRNA和蛋白质水平。此外，miR-let-7a的过表达显著抑制3T3-L1和D12细胞的生长，并降低HMGA2的mRNA和蛋白质水平。miR-let-7a抑制剂拮抗EGCG对3T3-L1和D12细胞数量和活力的抑制作用。此外，miR-let-7a抑制剂逆转了EGCG诱导的miR-let-7a表达水平升高以及HMGA2的mRNA和蛋白质水平降低。HMGA2的过表达导致细胞数量和活力增加，并拮抗EGCG抑制的3T3-L1和D12前脂肪细胞的生长和HMGA2表达。
EGCG通过调节miR-let-7a和HMGA2通路抑制3T3-L1和D12前脂肪细胞的生长。
