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Expression of PTEN, p27, p21 and AKT mRNA and protein in human BEL‐7402 hepatocarcinoma cells in transplanted tumors of nude mice treated with the tripeptide tyroservatide (YSV)
Author(s) -
Zhu Zhitong,
Jia Jing,
Lu Rong,
Lu Yi,
Fu Zheng,
Zhao Lan,
Wang Li,
Jin Mengjue,
Zhao Lin,
Gao Wenyuan,
Yao Zhi
Publication year - 2005
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.21501
Subject(s) - pten , protein kinase b , pi3k/akt/mtor pathway , oncogene , cancer research , western blot , tumor suppressor gene , biology , messenger rna , phosphorylation , microbiology and biotechnology , signal transduction , cancer , medicine , carcinogenesis , gene , cell cycle , biochemistry
The tripeptide, tyroservatide (YSV), has been previously shown to have antitumor effects through unknown mechanism. In the current study, we examined whether YSV modulates the protumorigenic PI3K pathway in human BEL‐7402 hepatocarcinoma cells. BEL‐7402 hepatocarcinoma was transplanted into the subcutaneous tissues of nude mice, and YSV, at varying doses, was administered. RT‐PCR and Western blot were used to analyze the expression of PTEN, AKT, p21 and p27. YSV at doses of 80 μg/kg/day, 160 μg/kg/day and 320 μg/kg/day markedly inhibited the growth of human BEL‐7402 hepatocarcinoma ( p < 0.05). YSV increased mRNA and protein expression of the tumor‐suppressor genes, PTEN , p21 and p27 , and inhibited the mRNA and protein expression of the oncogene AKT . Furthermore, YSV administration was associated with dephosphorylation of both PTEN (which activates PTEN) and AKT (which inhibits AKT). These results are consistent with the possibility that YSV mediates inhibition of tumor growth through inhibition of the PI3K pathway and suggests that YSV should be explored for use as an antitumor agent for hepatocarcinoma. © 2005 Wiley‐Liss, Inc.