Aloe emodin Inhibits Proliferation and Promotes Apoptosis in Non-Small Cell Lung Carcinoma (NSCLC) Cells by Deactivating PI3K/Akt/mTOR Signaling Pathways

Non-small cell lung cancer (NSCLC) accounts for approximately 85% of lung cancer cases and is often detected at advanced stages, limiting treatment options and adversely affecting patient outcomes.Recognized by the WHO as the leading cause of cancer-related deaths, NSCLC necessitates improved diagnostic and therapeutic strategies.Aloe-emodin (AE), a natural compound with known anticancer properties, has demonstrated efficacy in inducing apoptosis and inhibiting cell proliferation in various cancer types.This study investigates AE's potential in treating NSCLC by targeting the PI3K/Akt/mTOR signalling pathway, crucial for cancer cell survival and proliferation.A549 lung cancer cells were treated with varying concentrations of AE, and cell viability was assessed using the MTT assay.Molecular docking studies were conducted to explore AE's interactions with PI3K, Akt1, and mTOR.Gene expression levels of these proteins were analysed using RT-PCR.Results showed a concentrationdependent decrease in NSCLC cell viability, with significant reductions observed at 72 hours.RT-PCR analysis indicated the downregulation of PI3K, Akt1, and mTOR in AE-treated cells.Docking studies revealed strong binding affinities of AE to PI3K, suggesting its inhibitory potential.These findings highlight AE's promise as a therapeutic agent against NSCLC, warranting further investigation into its mechanisms and clinical applicability.