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.
Keyphrases
- cell cycle arrest
- induced apoptosis
- cell death
- endoplasmic reticulum stress
- oxidative stress
- pi k akt
- rna seq
- pet ct
- single cell
- signaling pathway
- endothelial cells
- high resolution
- poor prognosis
- squamous cell carcinoma
- papillary thyroid
- climate change
- mass spectrometry
- newly diagnosed
- lymph node metastasis
- bioinformatics analysis