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Induction of TSC-22 by Treatment with a New Anti-cancer Drug, Vesnarinone, in a Human Salivary Gland Cancer Cell

Overview
Journal Br J Cancer
Specialty Oncology
Date 1998 Feb 12
PMID 9459148
Citations 14
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Abstract

We undertook the present study to clarify the molecular mechanism of the effect of a new anti-cancer drug, vesnarinone, on a human salivary gland cancer cell line, TYS. We isolated TSC-22cDNA as avesnarinone-inducible gene from a cDNA library constructed from vesnarinone-treated TYS cells. TSC-22 was originally reported as a transforming growth factor (TGF)-beta-inducible gene. The expression of TSC-22 was up-regulated within a few hours after treatment with vesnarinone and was continued for 3 days. The level of TSC-22 mRNA in TYS cells was continuously increased until the cells reached confluency. Furthermore, the induction of TSC-22 by vesnarinone was inhibited by treatment with cycloheximide. When we treated the cells with an antisense oligonucleotide against TSC-22 mRNA under quiescent conditions, the antisense oligonucleotide stimulated the growth of TYS cells; however, under growing conditions the antisense oligonucleotide did not affect cell growth. Furthermore, the antisense oligonucleotide suppressed the antiproliferative effect of vesnarinone. These results suggest that TSC-22 may be a negative growth regulator and may play an important role in the antiproliferative effect of vesnarinone.

Citing Articles

Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.

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TSC-22 inhibits CSF-1R function and induces apoptosis in cervical cancer.

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Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.

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Overexpression of TSC-22 (transforming growth factor- β-stimulated clone-22) causes marked obesity, splenic abnormality and B cell lymphoma in transgenic mice.

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TSC-22 up-regulates collagen 3a1 gene expression in the rat heart.

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