Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/16893
Title: Inactivation mechanisms and growth suppressive effects of p16INK4a in Asian esophageal squamous carcinoma cell lines
Authors: Kwong, FM
Tang, JCO 
Srivastava, G
Lung, ML
Issue Date: 2004
Source: Cancer letters, 2004, v. 208, no. 2, p. 207-213
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.
Keywords: Esophageal squamous cell carcinoma
p16INK4a
Promoter hypermethylation
Transfection
Journal: Cancer Letters 
ISSN: 0304-3835
DOI: 10.1016/j.canlet.2003.11.017
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