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Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway
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Oridonin inhibits oral cancer growth and PI3K/Akt signaling pathway

Jing Yang1, Xianyue Ren1, Liping Zhang1

  • 1Guanghua School of Stomatology, Guangdong Provincial Key Laboratory of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|February 13, 2018
PubMed

Insights

Oridonin, a natural compound, effectively combats oral cancer by inhibiting cell growth, promoting apoptosis, and halting cell cycle progression. It targets key signaling pathways, showing promise as an oral cancer therapeutic.

Area of Science:

  • Pharmacology
  • Molecular Biology
  • Oncology

Background:

  • Oridonin, derived from Rabdosia rubescens, exhibits anticancer properties in various cancer types.
  • The therapeutic potential of oridonin against oral squamous cell carcinoma (OSCC) remains largely unexplored.

Purpose of the Study:

  • To investigate the anticancer effects of oridonin on OSCC cells.
  • To elucidate the underlying molecular mechanisms of oridonin's action in OSCC.

Main Methods:

  • Utilized OSCC cell lines (UM1 and SCC25) for in vitro studies.
  • Assessed proliferation, apoptosis, cell cycle distribution, and protein expression via Western blot.
  • Evaluated the impact of oridonin on PI3K/Akt signaling pathway.
  • Investigated oridonin's efficacy in an in vivo OSCC xenograft mouse model.

Main Results:

  • Oridonin significantly inhibited OSCC cell proliferation, clonal formation, and induced G2/M cell cycle arrest.
  • Treatment with oridonin promoted apoptosis by altering Bax/Bcl-2 ratios and activating caspases (caspase-3, caspase-9) and PARP-1.
  • Oridonin modulated G2/M transition proteins (down-regulating cyclin B1; up-regulating cyclin D1, D3, P21, p-CDK1, cyclin A2).
  • Oridonin suppressed PI3K/Akt phosphorylation and reduced OSCC tumor growth in vivo.

Conclusions:

  • Oridonin demonstrates significant anti-oral cancer activity by inducing apoptosis and G2/M cell cycle arrest.
  • The PI3K/Akt signaling pathway is a key target for oridonin's therapeutic effects in OSCC.
  • Oridonin represents a promising candidate for the development of novel oral cancer treatments.
Keywords:
Anticancer abilityOral squamous cell carcinoma (OSCC)OridoninPI3K/Akt signaling

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