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The effects of galangin on the apoptosis and autophagy of gastric cancer NCI-N87 cells through regulating the AMPK/mTOR/ULK1 signaling pathway
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Abstract:
[Abstract] Objective: To investigate the effects and mechanisms of galangin (Gal) on the apoptosis and autophagy of gastric cancer NCI-N87 cells through regulating the AMPK/mTOR/ULK1 signaling pathway. Methods: Gastric cancer NCI-N87 cells were assigned into the control group, the dorsomorphin (DM, AMPK inhibitor) group, the Gal low-dose (Gal-L) group, the Gal high-dose (Gal-H) group, and the Gal-H + DM group. Cell proliferation, apoptosis, migration, and invasion abilities were detected using MTT assay, flow cytometry, wound healing assay, and Transwell assay, respectively. Western blotting was used to detect the expression levels of PCNA, cleaved caspase-3 (C-caspase-3), immune evasion-related protein (B7H1), EMT, and AMPK/mTOR/ULK1 signaling pathway proteins. A NCI-N87 cell xenograft tumor model was established in nude mice to observe the inhibitory effects of Gal and 5-FU on the growth of transplant tumors. Results: Compared with the control group, the DM group exhibited significantly increased proliferation activity, scratch healing rate, number of invasive cells, and protein expression levels of N-cadherin, vimentin, PCNA, B7H1, p62, and p-mTOR/ mTOR in NCI-N87 cells (all P < 0.05), along with significantly decreased apoptosis rate and protein expression levels of C-caspase-3, E-cadherin, LC3Ⅱ/LC3Ⅰ, p-AMPK/AMPK, and p-ULK1/ULK1 (all P < 0.05). In contrast, both the Gal-L and Gal-H groups showed significantly decreased proliferation activity, scratch healing rate, number of invasive cells, and protein expression levels of N-cadherin, vimentin, PCNA, B7H1, p62, and p-mTOR/mTOR in NCI-N87 cells (all P < 0.05), while displaying significantly increased apoptosis rate and protein expression levels of C-caspase-3, E-cadherin, LC3Ⅱ/LC3Ⅰ, p-AMPK/AMPK, and p-ULK1/ULK1 (all P < 0.05). DM could partially reverse the inhibitory effect of Gal on the malignant biological behaviors of NCI-N87 cells (P < 0.05). Compared with the control group, both the Gal group and the 5-FU group exhibited significant reductions in tumor volume and mass, as well as a significant increase in the apoptosis rate of tumor tissue cells in nude mice (P < 0.05). Conclusion: Gal can promote the autophagy and apoptosis in gastric cancer NCI-N87 cells, inhibit their proliferation, migration, and invasion, which may be related to the activation of the AMPK/mTOR/ULK1 signaling pathway.
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