Control of AMP-activated Protein Kinase, Akt, and mTOR in EGCG-treated HT-29 Colon Cancer Cells

被引：11

作者：

Park, Song Yi ^{[2
]}

Lee, Yun-Kyoung ^{[4
]}

Kim, Young-Min ^{[2
]}

Park, Ock Jin ^{[3
]}

Shin, Jang-In ^{[1
]}

机构：

[1] Dankook Univ, Dept Oral Physiol, Sch Dent, Cheonan 330714, Chungnam, South Korea

[2] Hannam Univ, Dept Biol Sci & Biotechnol, Taejon 305811, South Korea

[3] Hannam Univ, Dept Food & Nutr, Taejon 305811, South Korea

[4] Suny Downstate Med Ctr, Dept Cell Biol, Brooklyn, NY 11203 USA

来源：

FOOD SCIENCE AND BIOTECHNOLOGY | 2013年 / 22卷 / 01期

关键词：

epigallocatechin-3-gallate; AMP-activated protein kinase; mTOR; Akt; colon cancer; INDEPENDENT MECHANISMS; BREAST-CANCER; PATHWAY; PHOSPHORYLATION; PROLIFERATION; GROWTH; TARGET;

D O I：

10.1007/s10068-013-0020-1

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Suppressing the mammalian target of rapamycin (mTOR) pathway has emerged as an attractive method for controlling cancer growth and preventing cancers. Epigallocatechin-3-gallate (EGCG) is a well-known chemo-preventive polyphenol, and its effects on AMP-activated protein kinase (AMPK) activation were previously reported. In this study the regulatory mechanisms of EGCG on mTOR and Akt, 2 cancer survival signals, and the interrelationships among mTORC1, Akt, and AMPK were examined. It was found that the suppression of mTORC1 by EGCG requires signals from AMPK, however, the inhibition of Akt with EGCG seems to be AMPK independent. Further, there was no clear indication of Akt as an upstream regulator of mTOR in EGCG treated HT-29 colon cancer cells.

引用

页码：147 / 151

页数：5

共 22 条

[1] The two TORCs and Akt [J].

Bhaskar, Prashanth T. ;

Hay, Nissim .

DEVELOPMENTAL CELL, 2007, 12 (04) :487-502

[2] The PKB/AKT Pathway in Cancer [J].

Carnero, Amancio .

CURRENT PHARMACEUTICAL DESIGN, 2010, 16 (01) :34-44

[3] Insulin and IGF-1 stimulate the β-catenin pathway through two signalling cascades involving GSK-3β inhibition and Ras activation [J].

Desbois-Mouthon, C ;

Cadoret, A ;

Blivet-Van Eggelpoël, MJ ;

Bertrand, F ;

Cherqui, G ;

Perret, C ;

Capeau, J .

ONCOGENE, 2001, 20 (02) :252-259

[4] Mammalian target of rapamycin is a biomarker of poor survival in metastatic serous ovarian carcinoma [J].

Elstrand, Mari Bunkholt ;

Dong, Hiep Phuc ;

Odegaard, Elin ;

Holth, Arild ;

Elloul, Sivan ;

Reich, Reuven ;

Trope, Claes G. ;

Davidson, Ben .

HUMAN PATHOLOGY, 2010, 41 (06) :794-804

[5] IGF1-induced AKT phosphorylation and cell proliferation are suppressed with the increase in PTEN during luteinization in human granulosa cells [J].

Goto, Maki ;

Iwase, Akira ;

Harata, Toko ;

Takigawa, Sachiko ;

Suzuki, Kyosuke ;

Manabe, Shuichi ;

Kikkawa, Fumitaka .

REPRODUCTION, 2009, 137 (05) :835-842

[6] AMPK phosphorylation of raptor mediates a metabolic checkpoint [J].

Gwinn, Dana M. ;

Shackelford, David B. ;

Egan, Daniel F. ;

Mihaylova, Maria M. ;

Mery, Annabelle ;

Vasquez, Debbie S. ;

Turk, Benjamin E. ;

Shaw, Reuben J. .

MOLECULAR CELL, 2008, 30 (02) :214-226

[7] TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling [J].

Inoki, K ;

Li, Y ;

Zhu, TQ ;

Wu, J ;

Guan, KL .

NATURE CELL BIOLOGY, 2002, 4 (09) :648-657

[8]

Kuhajda FP., 2008, INT J OBESITY, V4, P36

[9] Curcumin Exerts Antidifferentiation Effect through AMPKα-PPAR-γ in 3T3-L1 Adipocytes and Antiproliferatory Effect through AMPKα-COX-2 in Cancer Cells [J].

Lee, Yun K. ;

Lee, Won S. ;

Hwang, Jin T. ;

Kwon, Dae Y. ;

Surh, Young J. ;

Park, Ock J. .

JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2009, 57 (01) :305-310

[10] Suppression of mTOR via Akt-dependent and -independent mechanisms in selenium-treated colon cancer cells: involvement of AMPKα1 [J].

Lee, Yun-Kyoung ;

Park, Song Yi ;

Kim, Young-Min ;

Kim, Dong Chool ;

Lee, Won Sup ;

Surh, Young-Joon ;

Park, Ock Jin .

CARCINOGENESIS, 2010, 31 (06) :1092-1099

← 1 2 3 →