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Pin1 gene mutation is a rare event in gastric cancer
Author(s) -
KIM CHANG JAE,
SONG JAE HWI,
CHO YONG GU,
CHAE HIUN SUK,
NAM SUK WOO,
YOO NAM JIN,
LEE JUNG YOUNG,
PARK WON SANG
Publication year - 2006
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2006.apm_379.x
Subject(s) - pin1 , mutation , mutant , peptidylprolyl isomerase , transfection , biology , missense mutation , cancer research , gene , hek 293 cells , cancer , prolyl isomerase , microbiology and biotechnology , genetics , isomerase
The peptidyl‐prolyl isomerase Pin1 is strikingly overexpressed in human cancers and is a novel regulator of β‐catenin. To determine whether somatic mutation of the Pin1 gene is involved in the development and/or progression of gastric cancer, we searched for mutations of the Pin1 gene in 95 gastric cancer specimens. The effect of Pin1 on β‐catenin expression was further examined in wild‐ and mutant‐type Pin1 ‐transfected HEK 293T cells. We found only one missense mutation that led to the substitution of alanine by aspartic acid at codon 118 of the Pin1 gene. On transfection study, the mutant Pin1 showed an increased expression of β‐catenin. However, the mutation had no effect on expression of the Pin1 protein in the case with Pin1 mutation. These results suggest that Pin1 may not play a role in the development or progression of gastric cancer.