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Dioscin inhibits SCC15 cell proliferation via the RASSF1A/MST2/YAP axis

Hui Tian1, Xiyan Chen1, Yafei Zhang1

  • 1Department of Implantology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.

Molecular Medicine Reports
|March 31, 2021
PubMed

Insights

Dioscin, a natural compound, inhibits oral squamous cell carcinoma (OSCC) growth by activating RASSF1A, leading to YAP phosphorylation and promoting cell death. This suggests dioscin

Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Dioscin, derived from traditional Chinese herbs, exhibits anti-tumor properties.
  • The specific mechanisms of dioscin's effects on oral squamous cell carcinoma (OSCC) remain unclear.

Purpose of the Study:

  • To investigate the impact of dioscin on OSCC cell proliferation.
  • To elucidate the molecular pathways involved in dioscin's anti-cancer effects in OSCC.

Main Methods:

  • Cell Counting Kit-8 and 5-ethynyl-2'-deoxyuridine assays for proliferation.
  • Flow cytometry for cell cycle and apoptosis analysis.
  • Western blotting and co-immunoprecipitation for protein expression.

Main Results:

  • Dioscin significantly inhibited SCC15 cell proliferation, induced cell cycle arrest, and increased apoptosis.
  • Dioscin activated the tumor suppressor Ras association domain-containing protein 1A (RASSF1A) and phosphorylated oncoprotein Yes-associated protein (YAP).
  • YAP modulation affected dioscin's inhibitory impact, confirming its role in the observed effects.

Conclusions:

  • Dioscin upregulates RASSF1A in OSCC cells, leading to YAP phosphorylation and reduced transcriptional coactivation.
  • This mechanism enhances cell cycle arrest and apoptosis, ultimately inhibiting OSCC cell proliferation.
  • Dioscin shows potential as a therapeutic agent for oral squamous cell carcinoma.
Keywords:
dioscinyes‑associated proteinRas association domain‑containing protein 1Aproliferation

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