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Inactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines.

Abstract：

:The inactivation mechanisms and functional role of p16INK4a in three Asian esophageal squamous cell carcinoma (ESCC) cell lines were investigated by polymerase chain reaction (PCR) amplification, DNA sequencing, methylation-specific PCR analysis, reverse transcription-PCR, Western blotting, and colony formation assays. The p16INK4a was inactivated by promoter hypermethylation in all three cell lines, a homozygous deletion of exons 2 and 3, and a frameshift deletion on exon 1, leading to transcriptional silencing or the production of mutant p16INK4a protein. Two ESCC cell lines transfected with wild type p16INK4a show significantly reduced cell growth properties. The results of the present studies support the suppressive role of p16INK4a in ESCC development.

journal_name

Cancer Lett

journal_title

Cancer letters

authors

Kwong FM,Tang JC,Srivastava G,Lung ML

doi

10.1016/j.canlet.2003.11.017

keywords:

subject

Has Abstract

pub_date

2004-05-28 00:00:00

pages

207-13

issue

2

eissn

0304-3835

issn

1872-7980

pii

S0304383503008097

journal_volume

208

pub_type

杂志文章

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