PLCE1 suppresses p53 expression in esophageal cancer cells.

Abstract

The apoptotic mechanism dysfunction plays a critical role in cancer cell growth and escaping from cancer therapies; the underlying mechanisms are to be further elucidated. This study aims to investigate the role of phospholipase C epsilon 1 (PLCE1) in modulating the apoptosis mechanism in esophageal cancer (Eca) cells. The results showed that Eca cell lines, OE33 and CP-C cells expressed high levels of PLCE1. Knockdown of PLCE1 markedly increased 9.26 folds of the expression of p53 and 13.8 folds of the frequency of apoptotic CP-C cells via modulating the p53 promoter methylation.

• Authors: Yun Li, Jun An, Shaohong Huang, Hongying Liao, Yimin Weng, Songwang Cai, Junhang Zhang
• Journal: Cancer investigation (Cancer Invest) Vol. 32 Issue 6 Pg. 236-40 (Jul 2014) ISSN: 1532-4192 [Electronic] England
• PMID: 24766303 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• TP53 protein, human
• Tumor Suppressor Protein p53
• Phosphoinositide Phospholipase C
• phospholipase C epsilon

Topics

• Apoptosis (genetics)
• Carcinoma, Squamous Cell (genetics, metabolism, pathology)
• Cell Line, Tumor
• DNA Methylation (genetics)
• Esophageal Neoplasms (genetics, metabolism, pathology)
• Gene Expression Regulation, Neoplastic
• Gene Knockdown Techniques
• Humans
• Phosphoinositide Phospholipase C (genetics, metabolism)
• Promoter Regions, Genetic
• Tumor Suppressor Protein p53 (biosynthesis, genetics)