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

Curr Pharm Des. 2023;29(5):368-378. doi: 10.2174/1381612829666230130141931.


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.

Keywords: Scutellarin; Wnt/β-catenin signaling pathway; apoptosis; chemotherapy; gastric cancer; radiotherapy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis
  • Cell Line, Tumor
  • Cell Proliferation
  • Humans
  • Stomach Neoplasms* / drug therapy
  • Wnt Signaling Pathway*
  • beta Catenin / metabolism
  • beta Catenin / pharmacology


  • beta Catenin
  • scutellarin