Ailanthone Inhibits Cell Proliferation in Tongue Squamous Cell Carcinoma via PI3K/AKT Pathway

Area of Science:

• Oncology
• Pharmacology
• Molecular Biology

Background:

• Tongue squamous cell carcinoma (TSCC) is an aggressive oral cancer subtype with high recurrence rates.
• Ailanthone (AIL), derived from *Ailanthus altissima*, is investigated for its therapeutic potential.
• Understanding AIL's mechanism in TSCC is crucial for targeted treatment development.

Purpose of the Study:

• To investigate the anti-cancer effects of Ailanthone (AIL) on human tongue squamous cell carcinoma (TSCC) cell lines.
• To elucidate the molecular mechanisms underlying AIL's inhibitory effects on TSCC proliferation and viability.
• To evaluate AIL's potential as a therapeutic agent for TSCC.

Main Methods:

• Cell viability assays (e.g., MTT) were used to assess AIL's impact on Cal-27 and Tca8113 cell lines.
• Apoptosis was detected using Hoechst 33258 staining and flow cytometry analysis of apoptotic cell populations.
• Western blotting was employed to analyze the expression levels of key proteins involved in apoptosis (Bcl-2, Bax, PARP1, caspases) and cell cycle regulation (CDK1, cyclin B1), as well as the PI3K/Akt pathway.

Main Results:

• AIL significantly reduced the viability and proliferation of human TSCC cell lines (Cal-27, Tca8113).
• AIL treatment induced apoptosis, evidenced by increased early and late apoptotic cells and altered expression of apoptosis-related proteins (decreased Bcl-2/Bax ratio, PARP1, caspase-9, caspase-3; increased cleaved forms).
• AIL caused G2/M cell cycle arrest by downregulating CDK1 and cyclin B1, and inhibited the PI3K/Akt signaling pathway.

Conclusions:

• Ailanthone exhibits potent anti-proliferative and pro-apoptotic effects on tongue squamous cell carcinoma cells.
• AIL-induced cell cycle arrest at G2/M and PI3K/Akt pathway inhibition contribute to its anti-cancer activity.
• Ailanthone demonstrates significant potential for the development of novel therapeutic strategies against TSCC.