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Curcumin inhibits gastric cancer growth via downregulation of zinc finger protein, ZNF139
Abstract
Purpose: To investigate the effect of curcumin on gastric cancer cell proliferation and the mechanism of action involved.
Methods: Viability of gastric cells following curcumin treatment was determined by 3 (4,5 dimethyl thiazol 2 yl) 2,5 diphenyl 2H tetrazolium bromide (MTT) assay. Flow cytometry was used for the assessment of apoptosis induction in SGC 7901 cells. Reverse transcriptase polymerase chain reaction (RT-PCR) and western blotting assay were used for the analysis of Znf139, survivin and Bcl 2 protein expressions.
Results: The results showed that curcumin treatment reduced the viability of gastric cancer cell line SGC 7901 cells at 30 µM concentration to 29.67 % after 48 h compared to 99.78 % for control culture. Apoptotic cell population increased significantly (p < 0.05) following treatment with curcumin. Zinc finger protein-139 mRNA and protein expression decreased significantly (p < 0.05) on treatment with curcumin. Furthermore, curcumin suppressed the levels of B cell lymphoma 2 (Bcl 2) and survivin protein. In the mice model of gastric cancer, treatment with 50 mg/kg dose of curcumin inhibited tumor growth and development significantly, compared to the untreated group (p < 0.05).
Conclusion: The results demonstrate that curcumin treatment inhibits gastric cancer cell proliferation via down-regulation of zinc finger protein-139. It also suppresses tumor growth in mice. Therefore, curcumin is a promising gastric cancer inhibitor and should be further investigated for the management of gastric cancer.