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Updated: Jul 4, 2026
Isolation and Characterization of a Head and Neck Squamous Cell Carcinoma Subpopulation Having Stem Cell Characteristics
Published on: May 11, 2016
Characterization of homozygous deletions in laryngeal squamous cell carcinoma cell lines
Maciej Giefing1, Jose Ignacio Martin-Subero, Katarzyna Kiwerska
1Institute of Human Genetics, Polish Academy of Sciences, ul. Strzeszyńska 32, 60-479 Poznan, Poland. gifciu@wp.pl
Abstract:
The majority of classical tumor suppressor genes, such as CDKN2A or RB1, were identified by delineation of biallelic losses called homozygous deletions. To systematically identify homozygous deletions in laryngeal squamous cell carcinoma and to unravel novel putative tumor suppressor genes we screened three laryngeal squamous cell carcinoma cell lines (LSCC) using array comparative genomic hybridization (array-CGH). Out of 31 candidate regions for homozygous deletions identified by array-CGH, 5 were verified further by PCR. Among others, these homozygous deletions affected the tumor suppressor gene CDKN2A and the apoptosis-inducing STK17A gene. To assess the frequency of the identified deletions we investigated the affected sites in 9 additional LSCC cell lines. In 5 of the 9 cell lines the CDKN2A gene was homozygously lost. Thus, CDKN2A was homozygously deleted in 7 of the 12 cell lines. No other recurrent homozygous deletions were found. Homozygous deletions was a frequent mechanism of CDKN2A inactivation. Moreover, we identified several other genes, including the putative tumor suppressor gene STK17A, which may be inactivated by homozygous deletions and thus are potentially implicated in laryngeal squamous cell carcinoma development.
Insights
Researchers screened laryngeal squamous cell carcinoma cell lines for homozygous deletions, identifying CDKN2A inactivation as frequent. This study highlights STK17A as a potential tumor suppressor gene in laryngeal cancer development.
Area of Science:
- Oncology
- Genetics
- Genomics
Background:
- Classical tumor suppressor genes are often identified through homozygous deletions.
- Laryngeal squamous cell carcinoma (LSCC) requires systematic identification of such genes.
- Homozygous deletions are a key mechanism for tumor suppressor gene inactivation.
Purpose of the Study:
- To systematically identify homozygous deletions in LSCC.
- To discover novel putative tumor suppressor genes in LSCC.
- To determine the frequency of homozygous deletions for specific genes in LSCC.
Main Methods:
- Screening of three LSCC cell lines using array comparative genomic hybridization (array-CGH).
- Verification of candidate homozygous deletion regions using Polymerase Chain Reaction (PCR).
- Investigation of identified deletion sites in nine additional LSCC cell lines.
Main Results:
- Identified 31 candidate regions for homozygous deletions via array-CGH, with 5 verified by PCR.
- Confirmed homozygous deletions affecting the CDKN2A tumor suppressor gene and the STK17A gene.
- Found homozygous deletion of CDKN2A in 7 out of 12 LSCC cell lines, indicating frequent inactivation.
- No other recurrent homozygous deletions were identified across the cell lines.
Conclusions:
- Homozygous deletion is a prevalent mechanism for CDKN2A inactivation in LSCC.
- The STK17A gene, potentially a tumor suppressor, may be inactivated by homozygous deletions in LSCC.
- These findings implicate STK17A in the development of laryngeal squamous cell carcinoma.
