Penta-O-galloyl-β-D-glucose suppresses EGF-induced eIF3i expression through inhibition of the PI3K/AKT/mTOR pathway in prostate cancer cells

Victor Chia-Hsiang Lin; Po-Tsun Kuo; Ying-Chao Lin; Yeh Chen; You-Cheng Hseu; Hsin-Ling Yang; Jung-Yie Kao; Chi-Tang Ho; Tzong-Der Way

doi:10.1021/jf502447e

Penta-O-galloyl-β-D-glucose suppresses EGF-induced eIF3i expression through inhibition of the PI3K/AKT/mTOR pathway in prostate cancer cells

J Agric Food Chem. 2014 Sep 10;62(36):8990-6. doi: 10.1021/jf502447e. Epub 2014 Aug 29.

Authors

Victor Chia-Hsiang Lin¹, Po-Tsun Kuo, Ying-Chao Lin, Yeh Chen, You-Cheng Hseu, Hsin-Ling Yang, Jung-Yie Kao, Chi-Tang Ho, Tzong-Der Way

Affiliation

¹ Department of Urology, E-Da Hospital, I-Shou University , Kaohsiung, Taiwan.

PMID: 25123845
DOI: 10.1021/jf502447e

Abstract

Approximately 70% of prostate cancer patients will develop bone metastasis in axial and other regions of the skeleton. Epidermal growth factor (EGF) generated from bone tissue contributes to prostate cancer metastasis. In a previous study, penta-O-galloyl-β-D-glucose (PGG) suppressed androgen-independent prostate cancer bone metastasis by transcriptionally repressing EGF-induced MMP-9 expression. This study utilized proteomics to analyze the effects of PGG in EGF-induced prostate cancer bone metastasis. This study showed that PGG suppressed EGF-induced eIF3i expression in PC-3 cells. By transfection of eIF3i shRNA, it was observed that reduced eIF3i expression suppressed the invasion of PC-3 cells in vitro. PGG reduced EGF-induced eIF3i expression through inhibition of the PI3K/AKT/mTOR pathway. Therefore, PGG may be able to be used as a potential new therapeutic drug for prostate cancer bone metastasis.

Keywords: EGF; PGG; PI3K/AKT/mTOR; bone metastasis; prostate cancer.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Bone Neoplasms / prevention & control
Bone Neoplasms / secondary
Cell Line, Tumor
Epidermal Growth Factor / pharmacology
Eukaryotic Initiation Factor-3 / genetics*
Gene Expression / drug effects
Humans
Hydrolyzable Tannins / pharmacology*
Male
Neoplasm Metastasis / prevention & control
Phosphoinositide-3 Kinase Inhibitors*
Prostatic Neoplasms / metabolism*
Proto-Oncogene Proteins c-akt / antagonists & inhibitors*
RNA, Small Interfering / genetics
TOR Serine-Threonine Kinases / antagonists & inhibitors*
Transfection

Substances

Eukaryotic Initiation Factor-3
Hydrolyzable Tannins
Phosphoinositide-3 Kinase Inhibitors
RNA, Small Interfering
EIF3I protein, human
pentagalloylglucose
Epidermal Growth Factor
MTOR protein, human
Proto-Oncogene Proteins c-akt
TOR Serine-Threonine Kinases