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.
Scope: 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. Methods and results: 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 timeand 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. Conclusion: EGCG inhibits the growth of 3T3-L1 and D12 preadipocytes by modulating the miR-let-7a and HMGA2 pathways.
Prostate cancer (PC) and breast cancer (BC) are the most common cancers in men and women, respectively, in developed countries. The increased incidence of PC and BC largely reflects an increase in the prevalence of obesity and metabolic syndrome. In pathological conditions involving the development and progression of PC and BC, adipose tissue plays an important role via paracrine and endocrine signaling. The increase in the amount of local adipose tissue, specifically periprostatic adipose tissue, may be a key contributor to the PC pathobiology. Similarly, breast adipose tissue secretion affects various aspects of BC by influencing tumor progression, angiogenesis, metastasis, and microenvironment. In this context, the role of white adipose tissue (WAT) has been extensively studied. However, the influence of browning of the WAT on the development and progression of PC and BC is unclear and has received less attention. In this review, we highlight that adipose tissue plays a vital role in the regulation of the tumor microenvironment in PC or BC and highlight the probable underlying mechanisms linking adipose tissue with PC or BC. We further discuss whether the browning of WAT could be a therapeutic strategy for the treatment of PC and BC.
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