Scutellarin Suppressed Proliferation and Induced Apoptosis in Gastric Cancer via Wnt/beta-catenin Signaling Pathway

Background: Scutellarin exerts anticancer effects on diverse malignancies. However, its function in gastric cancer has not been explored. Objective: This study aimed to examine the anticancer effect and molecular mechanism of scutellarin in gastric cancer. Materials and Methods: Gastric cancer cells were treated with scutellarin and transfected with the Wnt1 overexpression plasmid. Cell viability, proliferation, toxicity, and apoptosis were determined by cell counting kit-8 (CCK-8), colony formation, lactate dehydrogenase (LDH) activity, TdT-mediated dUTP Nick-End Labeling (TUNEL), and flow cytometry assays. Expressions of apoptosis-related and Wnt/beta-catenin signaling pathway-related proteins were examined by western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR). Results: Scutellarin concentration dependently restrained cell viability. Scutellarin (20 and 80 mu mol/L) suppressed proliferation and promoted LDH release and apoptosis. Moreover, scutellarin elevated Bax and Cytochrome C levels but diminished the levels of Bcl-2, Wnt1, cytoplasmic beta-catenin, and basal cytoplasmic beta-catenin. However, the above-mentioned regulatory effects of scutellarin were all reversed by Wnt1 overexpression. Conclusion: Scutellarin suppressed gastric cancer cell proliferation and promoted apoptosis by inhibition of the Wnt/beta-catenin pathway.