Abstract
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/β-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 μmol/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 β-catenin, and basal cytoplasmic β-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/β-catenin pathway.
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