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Updated: Aug 20, 2026
Genome-Wide Analysis of DNA Methylation in Gastrointestinal Cancer
Published on: September 18, 2020
The clinical implication of 14-3-3 sigma expression in primary gastrointestinal malignancy
Kouji Tanaka1, Tsuyoshi Hatada, Minako Kobayashi
1The Second Department of Surgery, Mie University School of Medicine, 2-174 Edobashi, Tsu, Mie 514-8507, Japan.
Abstract:
14-3-3 Sigma is a checkpoint control gene that promotes G2 arrest following DNA damage. The inactivation of the 14-3-3 sigma gene, primarily by methylation-mediated silencing, has been reported in various human cancers. The loss of 14-3-3 sigma expression may contribute to malignant transformation by impairing the G2/M cell cycle checkpoint function, allowing an accumulation of genetic defects. In this report, we measured 14-3-3 sigma expression in 34 gastric and 35 colorectal cancers by using semi-quantitative reverse transcription-polymerase chain reaction and Western blot analysis. We also analyzed the association between 14-3-3 sigma expression and clinicopathological parameters including p53 status. Semi-quantitative reverse transcription-polymerase chain reaction and Western blot analysis showed that 14-3-3 sigma was significantly overexpressed in gastric and colorectal cancer tissues compared with normal ones (P<0.01). The immunoreactive 14-3-3 sigma protein was mainly detected in cytoplasm of cancer cells. Sigma overexpression tended to be associated with lymph node metastasis (P=0.08) in colorectal cancer. There was significant correlation between 14-3-3 sigma protein expression and the Ki-67 labeling index in gastric cancer (P=0.001). No significant association was observed between 14-3-3 sigma expression and p53 status. These results suggest that overexpressed 14-3-3 sigma in cancer cells might be induced by the p53 independent pathway, and that increased 14-3-3 sigma expression could contribute to cancer cell proliferation and the development and/or progression of human gastrointestinal cancers.
Insights
14-3-3 Sigma, a gene regulating cell cycle arrest, is overexpressed in gastric and colorectal cancers. This overexpression may drive cancer cell proliferation and progression through a p53-independent pathway.
Area of Science:
- Oncology
- Molecular Biology
- Cell Cycle Regulation
Background:
- 14-3-3 Sigma is a critical gene for G2 cell cycle arrest following DNA damage.
- Inactivation of 14-3-3 Sigma, often via methylation, is linked to various human cancers.
- Loss of 14-3-3 Sigma function may promote malignant transformation by disrupting cell cycle checkpoints.
Purpose of the Study:
- To investigate 14-3-3 Sigma expression levels in gastric and colorectal cancer tissues.
- To analyze the correlation between 14-3-3 Sigma expression and clinicopathological parameters, including p53 status.
Main Methods:
- Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to measure gene expression.
- Western blot analysis was employed to assess protein expression levels.
- Immunohistochemistry was utilized to determine protein localization within cancer cells.
Main Results:
- 14-3-3 Sigma was significantly overexpressed in both gastric and colorectal cancer tissues compared to normal tissues (P<0.01).
- Overexpressed 14-3-3 Sigma protein was predominantly found in the cytoplasm of cancer cells.
- A trend towards association between Sigma overexpression and lymph node metastasis was observed in colorectal cancer (P=0.08).
- Significant correlation was found between 14-3-3 Sigma protein expression and the Ki-67 labeling index in gastric cancer (P=0.001).
- No significant association was found between 14-3-3 Sigma expression and p53 status.
Conclusions:
- Overexpression of 14-3-3 Sigma in gastrointestinal cancers may occur independently of p53.
- Increased 14-3-3 Sigma expression is potentially linked to enhanced cancer cell proliferation.
- These findings suggest a role for 14-3-3 Sigma in the development and progression of human gastrointestinal cancers.
