Gallic acid suppresses colon cancer proliferation by inhibiting SRC and EGFR phosphorylation

xlomafota13 shared this article with you from Inoreader Gallic acid suppresses colon cancer proliferation by inhibiting SRC and EGFR phosphorylation Via Experimental and therapeutic medicine Exp Ther Med. 2021 Jun;21(6):638. doi: 10.3892/etm.2021.10070. Epub 2021 Apr 16. ABSTRACT The aim of the present study was to investigate the effects of gallic acid (GA) on the proliferation and apoptosis of colon cancer cells and to further clarify the mechanism of GA function associated with SRC and EGFR phosphorylation. HCT116 and HT29 cells were treated with different concentrations of GA for 24 h. Cell proliferation and apoptosis were analyzed using plate clone formation and flow cytometry assays, respectively. In addition, the expression of apoptosis-related proteins was examined by western blotting. Furthermore, the level of STAT3, AKT, SRC and EGFR phosphorylation was analyzed by western blotting and immunofluorescence. Subsequently, the SRC inhibitor PP2 and the EGFR inhibitor gefitinib were used to analyze the GA-associated mechanisms. In addition, a xenograft tumor model was established to confirm the effects of GA in viv o. The results indicated that GA inhibited cell proliferation and promoted cell apoptosis by upregulating the ratio of cleaved caspase-3/pro-caspase-3 and cleaved caspase-9/pro-caspase-9. Concurrently, GA decreased the level of phosphorylated (p)-SRC, p-EGFR, p-AKT and p-STAT3. Following treatment with PP2 and gefitinib in both cancer cell lines and animal model, GA was demonstrated to inhibit EGFR and SRC phosphorylation to downregulate STAT3 and AKT phosphorylation. In vivo, GA prevented tumor growth, promoted tumor apoptosis and decreased the level of p-SRC, p-EGFR, p-STAT3 and p-AKT. In conclusion, GA was indicated to suppress colon cancer proliferation by inhibiting SRC and EGFR phosphorylation. PMID:33968169 | PMC:PMC8097205 | DOI:10.3892/etm.2021.10070 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.