Impact of Phyllanthus emblica extract on A549 lung cancer cell malignancy via Akt/mTOR pathway

Abstract

Objective: To investigate the effects of Phyllanthus emblicaextract on the malignant biological behaviors of human non-small cell lung cancer A549 cells via the protein kinase B/mammalian target of rapamycin (Akt/mTOR) signaling pathway. Methods: Human non-small cell lung cancer A549 cells were selected and divided into a control group (blank treatment), low-dose Phyllanthus emblicaextract group (50 μ g/mL), medium-dose group (100 μ g/mL), high-dose group (200 μg/mL), and a positive control group (100 nmol/L rapamycin). Cell Counting Kit-8 (CCK-8) assays and flow cytometry were performed to evaluate cell viability and apoptosis, respectively. Transwell assays and wound healing assays were utilized to assess cell invasion and migration capacities. Western blotting was employed to detect the protein expression levels of Akt, p-Akt, mTOR, and p-mTOR. Additionally, a mouse xenograft model was established using A549 cells from each group to monitor tumor growth dynamics and survival rates. Results: Compared with the control group, tumor volume and weight in the low-, medium-, and high-dose extract groups and the positive control group were significantly reduced in a dose-dependent manner (all P< 0.05). Furthermore, cell viability, invasive and migratory abilities, as well as the protein expression levels of p-Akt and p-mTOR in the extract-treated groups and the positive control group were significantly lower than those in the control group (all P< 0.05). These inhibitory effects were more pronounced in the positive control and high-dose groups compared to the medium-dose group, and in the medium-dose group compared to the low-dose group (all P< 0.05). Conversely, the apoptosis rate of A549 cells increased in the extract-treated groups in a dose-dependent manner (all P< 0.05). Conclusion: Phyllanthus emblicaextract inhibits the activity of the Akt/mTOR signaling pathway. This inhibition interferes with the invasion and migration of lung cancer A549 cells, suppresses subcutaneous tumorigenesis in nude mice, and induces cellular apoptosis.