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

Author:

Chen Chia-Pei1,Su Tsung-Chen2,Yang Meei-Ju2,Chen Wen-Ting1,Siao An-Ci1,Huang Ling-Ru1,Lin Yen-Yue134,Kuo Yow-Chii5,Chung Jia-Fang6,Cheng Ching-Feng678,Ku Hui-Chen6,Kao Yung-Hsi1

Affiliation:

1. Department of Life Sciences, National Central University, Taoyuan 320

2. Tea Research and Extension Station, Council of Agriculture, Taoyuan 326

3. Department of Emergency Medicine, Taoyuan Armed Forces General Hospital, Taoyuan 325

4. Department of Emergency Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114

5. Department of Gastroenterology, Landseed Hospital, Taoyuan 324

6. Department of Pediatrics, Taipei Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, New Taipei City 23142

7. Institute of Biomedical Sciences, Academia Sinica, Taipei 11529

8. Department of Pediatrics, Tzu Chi University, Hualien 97004

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.

Funder

Tzu Chi General Hospital

Ministry of Science and Technology

Taoyuan Armed Forces General Hospital

National Central University and Landseed Hospital Joint Research

Publisher

SAGE Publications

Subject

General Biochemistry, Genetics and Molecular Biology

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