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