Mutation and aberrant expression of Caveolin-1 in human oral squamous cell carcinomas and oral cancer cell lines
Related Experiment Video
Updated: Aug 29, 2026

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
Published on: September 20, 2016
Song Ee Han1, Kyung-Hee Park, Gene Lee
1Department of Oral Biochemistry and Dental Research Institute, College of Dentistry Seoul National University, Seoul, Korea.
Abstract:
Caveolin-1, a tumor suppressor gene, was found to be inactivated by structural abnormalities or epigenetic changes in several types of human cancers. In order to investigate the role of Caveolin-1 in the pathogenesis of human oral squamous cell carcinoma, the exon 1 and 3 sequences of the Caveolin-1 were investigated in 74 oral squamous cell carcinomas and 15 oral cancer cell lines. In addition, Caveolin-1 expression was examined in 15 oral cancer cell lines. Mutations of the Caveolin-1 gene were identified in five cancers (1 missense and 4 silent mutations), with all mutations being detected in exon 3. Among the cancers containing the Caveolin-1 mutation, case 53 harbored a missense mutation from Ile (ATT) to Phe (TTT) at codon 141 and two silent mutations at codons 112 and 163 of the Caveolin-1 gene. Cases 27, 44, and 84 had two silent mutations from GAC (Asp) to GAT (Asp) at codon 82, and from CCA (Pro) to CCT (Pro) at codon 132. Case 89 contained three silent mutations at codons 84, 124, and 161. However, mutations of the Caveolin-1 gene were not observed in normal human oral keratinocytes, the human papillomavirus-immortalized oral keratinocytes, and 15 oral cancer cell lines. Despite the intact Caveolin-1 gene, one oral cancer cell line, HEp-2, lacked the caveolin-1 protein. In contrast, two cancer cell lines, KOSCC-25C and -33B, had an insignificant amount of the caveolin-1 protein. These results provide genetic evidence showing that the inactivation of Caveolin-1 by a mutation or by reduced expression may play a role in the pathogenesis of oral cancer.
Insights
Caveolin-1 gene mutations and reduced expression were found in oral cancers, suggesting its role in oral squamous cell carcinoma development. This tumor suppressor gene
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Caveolin-1 is a tumor suppressor gene frequently inactivated in various human cancers.
- Understanding Caveolin-1's role in oral cancer pathogenesis is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the mutation status and expression of the Caveolin-1 gene in human oral squamous cell carcinoma (OSCC).
- To determine the potential role of Caveolin-1 inactivation in OSCC development.
Main Methods:
- Sequencing of Caveolin-1 exons 1 and 3 in 74 OSCC samples and 15 oral cancer cell lines.
- Analysis of Caveolin-1 gene expression in 15 oral cancer cell lines.
- Comparison with normal oral keratinocytes and HPV-immortalized keratinocytes.
Main Results:
- Mutations in Caveolin-1 were identified in five OSCC samples, all located in exon 3.
- No Caveolin-1 mutations were found in normal oral keratinocytes or HPV-immortalized keratinocytes.
- Reduced or absent caveolin-1 protein expression was observed in some oral cancer cell lines despite intact genes.
Conclusions:
- Caveolin-1 gene mutations and reduced expression are implicated in the pathogenesis of oral squamous cell carcinoma.
- Inactivation of Caveolin-1, through mutation or decreased expression, may contribute to oral cancer development.
Related Concept Videos
Abnormal Proliferation
Cancers Originate from Somatic Mutations in a Single Cell
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Adaptive Mechanisms in Cancer Cells
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Cancer-Critical Genes II: Tumor Suppressor Genes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

