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The Tumor Suppressor Function of PTEN/MMAC1 through the Regulation of IGFs and IGFBPs

Korean Journal of Pediatrics 2004;47(8):884-891.
Published online August 15, 2004.
The Tumor Suppressor Function of PTEN/MMAC1 through the Regulation of IGFs and IGFBPs
Ho Keun Yi1, Dong Jin Hwang2, Sun Young Kim2, Dae Yeol Lee2, Pyoung Han Hwang2
1Department of Biochemistry, School of Dentistry, Chonbuk National University, Jeonju, Korea
2Department of Pediatrics, School of Medicine, Chonbuk National University, Jeonju, Korea
종양 세포주에서 IGFs와 IGFBPs의 제어를 통한 PTEN/MMAC1의 암억제 기능
이호근1, 황동진2, 김선영2, 이대열2, 황평한2
1전북대학교 치과대학 생화학교실
2전북대학교 의과대학 소아과학교실
Pyoung Han Hwang, Email: hwaph@chonbuk.ac.kr
: PTEN/MMAC1, a novel tumor suppressor gene, is mutated in a variety of advanced and metastatic cancers. It acts as a phosphatase, and thereby, regulates the PI-3 kinase/Akt pathway. In this study, we examined to evaluate the new function of anti-tumor effects of PTEN/MMAC1 through the regulation of the IGFs-IGFBPs in gastric cancer cells.
: PTEN/MMAC1 was expressed in an adenovirus-mediated gene delivery system and introduced into gastric cancer cells(SNU-484 & SNU-668) in vitro. The effect of cell growth and the expression of IGFs and IGFBPs after Ad/PTEN infection was analyzed by MTT assay, RT-PCR and Western immunoblot.
: Ad/PTEN infected cells were inhibited in cell growth compared with moak cells and Ad/ LacZ infected cells. Overexpression of PTEN/MMAC1 induced decrease in expression of IGF-I, -II and IGF-I receptors which are known as growth prompt molecules in a variety of cancers. Of the six IGFBPs, the expressions of IGFBP-4 and IGFBP-6 were decreased in Ad/PTEN infected cells. In contrast, IGFBP-3 expression was markedly increased by up to 3-fold in Ad/PTEN infected cells. Overexpression of PTEN/MMAC1 inhibited the activation of Akt/PKB pathway, but had no effect on the MAPK pathway.
: These findings suggest that the tumor suppressor function of PTEN/MMAC1 is, at least in part, mediated through the down-regulation of IGF-I abd IGF-II, and up-regulation of IGFBP-3 in gastric cancer cells by the inhibition of PI-3 kinase pathway.
Key Words: Genes, Tumor suppressor, Insulin-like growth factor I, Insulin-like growth factor II, Insulin-like growth-factor-binding proteins, Phosphatidylinositol 3-kinase, Stomach neoplasms

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