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Anticancer Res. 2010 Oct;30(10):3919-25.

Methylation-mediated silencing of TMS1 in pancreatic cancer and its potential contribution to chemosensitivity.

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1
Sylvester Cancer Center, University of Miami, Miami, Florida 33136, USA.

Abstract

BACKGROUND:

Resistance to chemotherapeutic agents, resulting in part from epigenetic silencing of pro-apoptotic genes, is one of the causes of treatment failure of pancreatic cancer. We examined whether epigenetic silencing of target of methylation induced silencing 1 (TMS1) contributes to resistance to chemotherapy in pancreatic cancer.

MATERIALS AND METHODS:

Methylation analysis was performed by methylation-specific PCR (MS-PCR) and gene expression was analyzed by quantitative reverse transcriptase PCR (qRT-PCR). MIA PaCa-2 cells were transfected with pCMV6-XL5/TMS1 plasmid and the effect of TMS1 expression on sensitivity to gemcitabine and docetaxel was determined. Cell viability was measured using Cell Titer Blue assay.

RESULTS:

TMS1 expression was repressed in MIA PaCa-2 cells by DNA methylation. Up-regulation of TMS1 by recombinant gene expression in MIA PaCa-2 cells or by pre-treatment of these cells with 5-azacytidine resulted in enhanced sensitivity to gemcitabine and docetaxel.

CONCLUSION:

Our results suggest that TMS1 is a potential therapeutic target in pancreatic cancer.

PMID:
21036703
[Indexed for MEDLINE]
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