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.
| Original language | English |
|---|---|
| Pages (from-to) | 207-213 |
| Number of pages | 7 |
| Journal | Cancer Letters |
| Volume | 208 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 28 May 2004 |
UN SDGs
This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- Esophageal squamous cell carcinoma
- p16INK4a
- Promoter hypermethylation
- Transfection
ASJC Scopus subject areas
- Cancer Research
- Molecular Biology
- Oncology
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