Effects of atranorin on the proliferation, apoptosis and metastasis of two different gastric cancer cell lines and exploring underlying mechanisms.

BACKGROUND

Gastric cancer is the fifth most prevalent malignancy worldwide. Atranorin is a polyphenol with significant anti-tumor activities. This study was conducted to evaluate the effect of atranorin on proliferation, apoptosis, and metastasis in two different human gastric cancer cell lines, AGS and HGC-27.

METHODS

The anti-proliferative and anti-migration effects of atranorin were evaluated using the MTT and scratch assays, respectively. The expression of apoptosis-related markers, including caspase 3, caspase 9, caspase 8, Bax, and Bcl2, and metastasis markers, including E-cadherin, N-cadherin, vimentin, fibronectin 1, and VEGFA, was quantified at the mRNA and protein levels via quantitative real-time PCR (qRT-PCR) and Western blotting, respectively.

RESULTS

Following exposure to varying concentrations of atranorin for 48 and 72 h, both cell lines exhibited a significant, dose-dependent decrease in cell proliferation compared with control groups. Atranorin treatment significantly increased the expression of caspase 3, caspase 9, and Bax in the HGC-27 cell line; conversely, no significant alterations were observed in the expression of caspase 8 and BCL2. In the AGS cell line, atranorin treatment did not significantly affect the expression of apoptosis markers. Atranorin induced apoptosis and inhibited migration in HGC-27 cells. Moreover, atranorin significantly upregulated E-cadherin and downregulated N-cadherin, vimentin, fibronectin 1, and VEGFA.

CONCLUSION

Atranorin inhibits proliferation in HGC-27 and AGS cells, induces intrinsic apoptosis, and inhibits metastasis in HGC-27 cells, suggesting its potential as a drug candidate, particularly for targeting metastasis and inducing apoptosis in highly metastatic HGC-27 cells.