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.
Keywords:
Apoptosis; Esophageal cancer; P53; Phospholipase C epsilon 1; Signal transducer and activator of transcription 3.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Apoptosis / genetics
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Carcinoma, Squamous Cell / genetics*
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Carcinoma, Squamous Cell / metabolism
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Carcinoma, Squamous Cell / pathology
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Cell Line, Tumor
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DNA Methylation / genetics
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Esophageal Neoplasms / genetics*
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Esophageal Neoplasms / metabolism
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Esophageal Neoplasms / pathology
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Gene Expression Regulation, Neoplastic
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Gene Knockdown Techniques
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Humans
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Phosphoinositide Phospholipase C / genetics
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Phosphoinositide Phospholipase C / metabolism*
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Promoter Regions, Genetic
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Tumor Suppressor Protein p53 / biosynthesis*
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Tumor Suppressor Protein p53 / genetics
Substances
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TP53 protein, human
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Tumor Suppressor Protein p53
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Phosphoinositide Phospholipase C
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phospholipase C epsilon