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Adiponectin-activated AMPK stimulates dephosphorylation of AKT through protein phosphatase 2A activation

Authors
 Kun-yong Kim  ;  Ahmi Baek  ;  Ji-Eun Hwang  ;  Yeon A. Choi  ;  Joon Jeong  ;  Myeong-Sok Lee  ;  Dea Ho Cho  ;  Jong-Seok Lim  ;  Keun Il Kim  ;  Young Yang 
Citation
 CANCER RESEARCH, Vol.69(9) : 4018-4026, 2009 
Journal Title
 CANCER RESEARCH 
ISSN
 0008-5472 
Issue Date
2009
MeSH
Adiponectin/pharmacology* ; Animals ; Breast Neoplasms/drug therapy ; Breast Neoplasms/enzymology* ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Cell Membrane/drug effects ; Cell Membrane/enzymology ; Enzyme Activation/drug effects ; Female ; Humans ; Isoenzymes ; Mice ; Mice, Inbred BALB C ; Neoplasm Metastasis ; Phosphorylation/drug effects ; Protein Kinases/metabolism* ; Protein Phosphatase 2/metabolism* ; Proto-Oncogene Proteins c-akt/metabolism*
Abstract
Low serum levels of adiponectin are a high risk factor for various types of cancer. Although adiponectin inhibits proliferation and metastasis of breast cancer cells, the underlying molecular mechanisms remain obscure. In this study, we show that adiponectin-activated AMPK reduces the invasiveness of MDA-MB-231 cells by stimulating dephosphorylation of AKT by increasing protein phosphatase 2A (PP2A) activity. Among the various regulatory B56 subunits, B56gamma was directly phosphorylated by AMPK at Ser(298) and Ser(336), leading to an increase of PP2A activity through dephosphorylation of PP2Ac at Tyr(307). We also show that both the blood levels of adiponectin and the tissue levels of PP2A activity were decreased in breast cancer patients and that the direct administration of adiponectin into tumor tissues stimulates PP2A activity. Taken together, these findings show that adiponectin, derived from adipocytes, negatively regulates the invasiveness of breast cancer cells by activating the tumor suppressor PP2A.
Files in This Item:
T200903639.pdf Download
DOI
10.1158/0008-5472.CAN-08-2641
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Surgery (외과학교실) > 1. Journal Papers
Yonsei Authors
Jeong, Joon(정준) ORCID logo https://orcid.org/0000-0003-0397-0005
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/105243
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