Green tea epigallocatechin gallate suppresses 3T3-L1 cell growth via microRNA-143/MAPK7 pathways

Abstract

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.

Dietary Epigenetic Modulators: Unravelling the Still-Controversial Benefits of miRNAs in Nutrition and Disease

“…The combined treatment of catechin epigallocatechin gallate (EGCG) and quercetin prevented insulin resistance by increasing the expression of miR-27a-3p and miR-96-5p, which directly target Forkhead Box O1 (FOXO1), reducing the production of glucose and the transcription of gluconeogenic enzymes [ 97 ]. In addition, ECGC showed therapeutic potential in obesity inhibiting white and beige 3T3-L1 and D12 preadipocyte growth by upregulated miR-let-7a and subsequent high-mobility group AT-hook 2 (HMGA2) suppression [ 98 ] and inhibiting the MAPK7 pathway by increased miR-143 levels [ 99 ]. Clinical data from a cohort of women affected by overweight and insulin resistance revealed that blood orange juice consumption (500 mL per day) for four weeks resulted in upregulated miR-144-3p, miR-424-5p, miR-144-3p, and miR-130b-3p and decreased let-7f-5p and miR-126-3p levels in peripheral blood mononuclear cells, leading to attenuated IL-6 and NF-κB mRNA expression [ 100 ].…”

Ferroptosis-Regulated Natural Products and miRNAs and Their Potential Targeting to Ferroptosis and Exosome Biogenesis

“…A detailed investigation of ferroptosis responses for these natural products and miRNAs is warranted. Curcumin [272] miR-125b-5p PEITC [273], quercetin [274], EGCG [275], berberine [276] miR-1287-5p Curcumin [277] miR-129-5p Matrine [278] miR-142-3p Artesunate [279], quercetin [280], curcumin [281] miR-143-3p Curcumin [282], EGCG [283,284], sulforaphane [285], quercetin [286] miR-144-3p Curcumin [287] miR-15a-5p Curcumin [288], baicalin [289], Withaferin A [290] miR-15a-3p EGCG [284] miR-205-5p Cryptotanshinone ↓ [291] proanthocyanidins ↓ [292], curcumin [293] miR-214-3p EGCG [284], sulforaphane [285] miR-25-3p Withaferin A [294] miR-27a-3p β-elemene [295], quercetin [296] miR-28-5p Curcumin [297] miR-302a-3p Curcumin [298] miR-324-3p Salinomycin ↓ [299] miR-365a-3p Sulforaphane [300] miR-375-3p Solasonine [301] miR-409-3p Curcumin [302] miR-429 Curcumin [303], berberine ↓ [304,305] miR-489-3p Curcumin [306] Ferroptosisinhibiting miRNAs miR-18a-5p Curcumin ↓ [307] miR-19a-3p Berberine [308], proanthocyanidins …”

“…Curcumin inhibits autophagy and enhances the radiosensitivity of prostate cancer cells by upregulating miR-143-3p [ 282 ]. EGCG inhibits the proliferation of preadipocytes [ 283 ] and breast cancer cells [ 284 ] by upregulating miR-143-3p. Additionally, gastric cancer cells express low levels of miR-143-3p.…”

“…It downregulates one ferroptosis-inhibiting miRNA (miR-18a-5p [ 307 ]). Similarly, EGCG upregulates four ferroptosis-inducing miRNAs (miR-125b-5p [ 275 ], miR-143-3p [ 283 , 284 ], miR-15a-3p [ 284 ], and miR-214-3p [ 284 ]) and downregulates one ferroptosis-inhibiting miRNA (miR-522-3p [ 284 ]). Matrine upregulates ferroptosis-inducing miRNA (miR-129-5p) [ 278 ] and downregulates ferroptosis-inhibiting miRNA (miR-19a-3p) [ 309 ].…”

A Strainer-Based Platform for the Collection and Immunolabeling of Mouse Intestinal Organoids

“…However, there remains deficiencies in both cell and animal research methodologies. Cell research normally focuses on one or several cellular components [5,6] and, thus, cannot well describe biological processes occurring in vivo. Despite animal research being able to reproduce various disease processes [7,8], issues such as long experimental periods [9], animal mortality [10], ethics [11], and economics [12] remain problematic.…”