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

Fung Mei Kwong, Cheuk On Tang, Gopesh Srivastava, Maria Li Lung

Research output: Journal article publicationJournal articleAcademic researchpeer-review

11 Citations (Scopus)


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.
Original languageEnglish
Pages (from-to)207-213
Number of pages7
JournalCancer Letters
Issue number2
Publication statusPublished - 28 May 2004


  • Esophageal squamous cell carcinoma
  • p16INK4a
  • Promoter hypermethylation
  • Transfection

ASJC Scopus subject areas

  • Cancer Research
  • Molecular Biology
  • Oncology

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