Boswellic acid exerts anti-tumor effect in oral squamous cell carcinoma by inhibiting PI3K/AKT1 mediated signaling pathway.

Abstract

Background: Boswellic acid (BA) is a bioactive compound derived from Boswellia trees. This study aims to investigate the anti-cancer properties of BA against KB oral squamous cancer cells and elucidate the underlying mechanisms.

Methods: Escalating doses of BA were administered to KB cells, and various analyses were conducted using bioinformatic tools such as GEO, GEO2R, and STITCH database. MTT and trypan blue assays has been validated to measure the cytotoxicity by treating BA in KB Cells. Flow cytometry assessed cell cycle progression, apoptosis induction, and metabolic alterations. Network analysis identified relevant signaling pathways, while RT-PCR validated mRNA expression changes. Docking studies by Autodock evaluated beta-BA's binding affinity with mTOR-mediated pathways.

Results: BA effectively hindered KB cell progression, inducing G0/G1 phase cell cycle arrest and apoptosis. It also inhibited aerobic glycolysis, a hallmark of oral cancer cells. Network analysis revealed involvement in apoptosis and mTOR targets. RT-PCR confirmed downregulation of genes associated with aerobic glycolysis and apoptosis. Docking studies indicated strong binding between BA and mTOR pathways.

Conclusions: BA shows promise in inhibiting KB oral squamous cancer cell growth. These findings underscore its potential as a treatment for oral cancer. Further research and clinical studies are needed to unlock its full therapeutic potential.