miR-206-3p Inhibits 3T3-L1 Cell Adipogenesis via the c-Met/PI3K/Akt Pathway

Abstract

MicroRNAs (miRNAs) are important post-transcriptional regulators during adipocyte adipogenesis. MiR-206-3p, a tissue-specific miRNA, is absent in white adipocytes. In this study, we examined the roles of mmu-miR-206-3p in the adipogenic differentiation of 3T3-L1 preadipocytes. The miR-206-3p expression has shown an apparent decreasing trend after induction, and sustained low expression throughout the differentiation of 3T3-L1 cells. miR-206-3p blocked the adipogenic differentiation of 3T3-L1 cells by attenuating c-Met expression; the inhibition effect of miR-206 to the adipogenic differentiation can be counteracted by restoring c-Met expression. In addition, miR-206-3p decreased the phosphorylation of Akt, which is the downstream effector of c-Met in the PI3K/Akt signaling pathway. These data indicate that miR-206-3p inhibits adipocyte adipogenesis through silencing c-Met and subsequently inactivating the PI3K/Akt signaling pathway.

Retracted Article: MiR-206 reduced the malignancy of hepatocellular carcinoma cells in vitro by inhibiting MET and CTNNB1 gene expressions

“…19,31 Inhibition of MET gene expression by miR-206 has been suggested to limit the development of various types of cancers. 9,11,[31][32][33][34][35] We found that miR-206 mimic transfection signicantly reduced c-Met protein level in patient-derived HCC cells, and restoring c-Met protein level by transient overexpression could partially restore the malignancy of HCC cells that were reduced by miR-206 mimic transfection in vitro, suggesting that inhibiting c-Met protein expression is implicated in the HCC-suppressive role of miR-206. We observed no signicant inuence on EGFR or IGF1R protein level in HCC cells by miR-206 mimic transfection (data not shown), although several previous reports have described the inhibition of EGFR gene expression by miR-206 via mRNA targeting in lung squamous cell carcinoma, 36 head and neck squamous cell carcinoma 37 and ovarian carcinoma cells.…”

Dual Effects of Metformin on Adipogenic Differentiation of 3T3-L1 Preadipocyte in AMPK-Dependent and Independent Manners

“…However, studies of the direct role of JNK in adipogenesis are scarce. In addition, the PI3K/Akt pathway is also essential for adipocyte differentiation [ 37 ]. It was reported that Akt overexpression promotes adipogenesis, and suppression of Akt has been shown to induce lipoatrophy and inhibit adipogenesis [ 37 , 38 , 39 ].…”

“…In addition, the PI3K/Akt pathway is also essential for adipocyte differentiation [ 37 ]. It was reported that Akt overexpression promotes adipogenesis, and suppression of Akt has been shown to induce lipoatrophy and inhibit adipogenesis [ 37 , 38 , 39 ]. Although many studies have examined the role of MAPKs and Akt signaling cascades in adipogenesis, to our knowledge, there are very few studies about the effects of metformin on these signaling pathways during adipogenesis.…”

Exercise Training-Induced Changes in MicroRNAs: Beneficial Regulatory Effects in Hypertension, Type 2 Diabetes, and Obesity

“…MiR-27b targets PPARγ, being reduced in obesity and increased after exercise [ 253 , 256 ]. MiR-206, which was shown to block adipogenesis [ 289 ], is reduced in the circulation of obese subjects, and increased after marathon runs in healthy subjects [ 290 ].…”