绿茶表没食子儿茶素没食子酸酯通过 microRNA-143/MAPK7 通路抑制 3T3-L1 细胞生长。
Green tea epigallocatechin gallate suppresses 3T3-L1 cell growth via microRNA-143/MAPK7 pathways.
机构信息
Department of Life Sciences, National Central University, Taoyuan 320.
Tea Research and Extension Station, Council of Agriculture, Taoyuan 326.
出版信息
Exp Biol Med (Maywood). 2022 Sep;247(18):1670-1679. doi: 10.1177/15353702221108925. Epub 2022 Jul 27.
Green tea epigallocatechin gallate (EGCG) and microRNA (miRNA) molecules modulate obesity. Nevertheless, it is still unknown whether EGCG modulates fat cell growth via miRNA-related signaling. In this study, white preadipocytes were used to examine whether the antimitogenic effect of EGCG on fat cells is regulated by the miR-143/MAPK7 pathway. We showed that EGCG upregulated the levels of miR-143, but not miR-155, in 3T3-L1 preadipocytes. Moreover, EGCG downregulated MAPK7 mRNA and protein levels time- and dose-dependently. MAPK7 expression increased during 3T3-L1 cell proliferation. miR-143 overexpression in the absence of EGCG mimicked the effects of EGCG to suppress preadipocyte growth and MAPK7 expression, whereas knockdown of miR-143 antagonized the EGCG-altered levels of miR-143, MAPK7, and pERK1/2 and reversed the EGCG-inhibited cell growth. These findings suggest that EGCG inhibits 3T3-L1 cell growth via miR-143/MAPK7 pathway.
绿茶表没食子儿茶素没食子酸酯（EGCG）和 microRNA（miRNA）分子调节肥胖。然而，EGCG 是否通过 miRNA 相关信号通路调节脂肪细胞生长仍不清楚。在这项研究中，使用白色前体脂肪细胞来检查 EGCG 对脂肪细胞的抗有丝分裂作用是否受 miR-143/MAPK7 途径调节。我们表明，EGCG 在 3T3-L1 前体脂肪细胞中上调 miR-143 的水平，但不上调 miR-155 的水平。此外，EGCG 以时间和剂量依赖的方式下调 MAPK7 mRNA 和蛋白水平。MAPK7 表达在 3T3-L1 细胞增殖过程中增加。在没有 EGCG 的情况下过表达 miR-143 模拟了 EGCG 抑制前体脂肪细胞生长和 MAPK7 表达的作用，而 miR-143 的敲低则拮抗了 EGCG 改变的 miR-143、MAPK7 和 pERK1/2 水平，并逆转了 EGCG 抑制的细胞生长。这些发现表明，EGCG 通过 miR-143/MAPK7 途径抑制 3T3-L1 细胞生长。
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