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The present study aimed to investigate the effects of perfluorooctanoic acid (PFOA) on tumor cell migration, invasion and apoptosis by activation of the PI3K/AKT signaling pathway in human rhabdomyosarcoma (RMS). PFOA is a persistent, synthetic organic environment pollutant, which has been previously associated with multiple diseases, including cancer. The present study aimed to confirm whether PFOA can elicit cell growth in the RD subline of RBS. RD cells were treated with different concentrations of PFOA. Cell proliferation was evaluated using Cell Counting Kit‑8 and cell cycle assays. Cell migration and invasion were determined using wound healing and Transwell assays. Apoptotic rates were estimated by Annexin V‑FITC/propidium iodide staining. The expression levels of vimentin, serum/glucocorticoid‑regulated kinase 1 (SGK1), cyclin E2, cyclin dependent kinase (CDK)2, p53, p21, p27, phosphatidylinositol‑3 kinase (PI3K) and protein kinase B (AKT), and apoptosis‑associated genes and proteins (including Bcl‑2 and Bax) were detected by reverse transcription‑PCR and western blot analyses. The results showed that PFOA significantly promoted RD cell proliferation, migration and invasion and significantly inhibited RD cell apoptosis. Exposure to PFOA also induced the expression of vimentin, SGK1, cyclin E2, CDK2, AKT, PI3K and Bcl‑2, but suppressed the expression of Bax in the RD cells. The treatment of RD cells with BEZ235, a PI3K inhibitor, antagonized the effects of PFOA on metastatic formation and apoptosis. The results obtained show that the PI3K/AKT signaling pathway is implicated in mediating the pro‑neoplastic effects of PFOA. The data suggests that PFOA is a carcinogen capable of promoting RD cell migration and invasion and inhibiting apoptosis through the PI3K/AKT signaling pathway.

Perfluorooctanoic acid induces migration and invasion and inhibits apoptosis through the PI3K/AKT signaling pathway in human rhabdomyosarcoma cells