Molecular biology reports · 2025
Effects of atranorin on the proliferation, apoptosis and metastasis of two different gastric cancer cell lines and exploring underlying mechanisms.
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Almuraikhi Nihal, Almasabi Saleh Hussain A, Alhazmi Abdulfattah Y, Almohammed Abdulrahman, Barnawi Jameel, Alghamdi Salah, Alhazmi Khalid
Аннотация
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.
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.