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• W2055781284 startingPage "3087" @default.
• W2055781284 abstract "The type II transforming growth factor (TGF)-β receptor gene ( TGFBR2 ) is often mutated in nucleotide repeat sequences in colorectal cancers that are replication error positive (RER+). These mutations are thought to be selected for escape from growth inhibition by TGF-β rather than representing bystander events because of an increased mutation rate. We investigated the role of TGFBR2 mutations in 12 colorectal cancer cell lines. Six of these were RER+, and these were shown to have homozygous TGFBR2 mutations. All cell lines then were tested for changes in proliferation in response to TGF-β stimulation. Despite homozygous mutation of the type II TGF-β receptor, two RER+ cell lines, Lovo and SW48, showed statistically significant growth inhibition when stimulated by TGF-β1 in serum-free conditions. This shows that the type II TGF-β receptor can be bypassed in certain cases to maintain growth inhibition. We next investigated whether there was any alternative mode through which TGFBR2 mutation may give a selective advantage, such as a change in adhesion molecule expression. All cell lines were stimulated with TGF-β1 and adhesion molecules detected by ELISA. No consistent changes were identified between the RER+ and the RER− cell lines, although changes in E-cadherin, β-catenin, and γ-catenin were identified in individual cell lines. We conclude that ( i ) type II TGF-β receptor activity can be bypassed and thus TGFBR2 mutations in RER+ cancers may, at least sometimes, be just “bystander” events and ( ii ) TGF-β can affect adhesion molecule expression so that TGFBR2 mutation may give rise to a selective advantage through an effect other escape from growth inhibition." @default.
• W2055781284 created "2016-06-24" @default.
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• W2055781284 date "1999-03-16" @default.
• W2055781284 modified "2023-09-23" @default.
• W2055781284 title "Transforming growth factor β stimulation of colorectal cancer cell lines: Type II receptor bypass and changes in adhesion molecule expression" @default.
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• W2055781284 doi "https://doi.org/10.1073/pnas.96.6.3087" @default.
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