Scutellarin Suppressed Proliferation and Induced Apoptosis in Gastric Cancer via Wnt/β-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/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.