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Published on: July 22, 2020
Transcriptome analysis reveals GA induced apoptosis in HCT116 human colon cancer cells through calcium and p53 signal
Chen Yang1,2,3, Xiaoyu Xie4, Hu Tang1,2,3
1Oil Crops Research Institute, Chinese Academy of Agricultural Sciences Wuhan 430062 P. R. China yangchen@caas.cn huangfh@oilcrops.cn.
Abstract:
Gallic acid (GA) is a polyphenol widely found in numerous fruits and vegetables that has been reported to exert anticancer effects, including apoptosis, against cancer cell lines. However, little is known about the induction of apoptotic effects and the underlying mechanism. We used RNA-seq to examine differentially expressed genes in human colon cancer HCT116 cells after 12 h and 24 h exposure to GA. A total of 792 and 911 genes with known functions showed significantly different expression levels in 12 h and 24 h GA-treated HCT116 cells, respectively. KEGG enrichment analysis showed that the identified genes were involved in pathways such as cholinergic synapse, circadian entrainment, calcium signal processing and transport, arachidonic acid metabolism and the p53 signal pathway. Real-time quantitative PCR was used to validate the reliability of the results obtained by RNA-seq. The results of this study indicate that GA triggers apoptosis in HCT116 cells through obstructing the growth of cells in the early phase treatment by down-regulation of calcium channels and then up-regulation of the intrinsic p53 signal pathway through activation of apoptosis caspases, finally leading to the mitochondrial apoptosis pathway.
Insights
Gallic acid (GA) induces colon cancer cell death by triggering apoptosis. This polyphenol down-regulates calcium channels and up-regulates the p53 pathway, ultimately activating the mitochondrial apoptosis pathway.
Area of Science:
- Molecular Biology
- Cancer Research
- Pharmacology
Background:
- Gallic acid (GA), a natural polyphenol, exhibits anticancer properties, including apoptosis induction in cancer cell lines.
- The precise mechanisms by which GA induces apoptosis remain largely unelucidated.
Purpose of the Study:
- To investigate the molecular mechanisms underlying gallic acid-induced apoptosis in human colon cancer HCT116 cells.
- To identify key genes and pathways affected by GA treatment using transcriptomic analysis.
Main Methods:
- RNA sequencing (RNA-seq) was employed to analyze gene expression changes in HCT116 cells after 12 and 24 hours of GA exposure.
- KEGG pathway enrichment analysis was performed to identify significantly altered biological pathways.
- Real-time quantitative PCR (RT-qPCR) was utilized to validate RNA-seq findings.
Main Results:
- GA treatment significantly altered the expression of 792 genes at 12 hours and 911 genes at 24 hours.
- Enriched pathways included cholinergic synapse, circadian entrainment, calcium signaling, arachidonic acid metabolism, and the p53 signaling pathway.
- GA treatment led to the down-regulation of calcium channels and subsequent up-regulation of the p53 signaling pathway.
Conclusions:
- Gallic acid effectively triggers apoptosis in HCT116 colon cancer cells.
- The mechanism involves initial cell growth obstruction via calcium channel down-regulation, followed by p53 pathway activation and caspase-mediated mitochondrial apoptosis.
- GA represents a potential therapeutic agent for colon cancer, warranting further investigation.
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