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Objective To investigate the effect of β-Elemene (β-Ele) on the cisplatin sensitivity of OSCC cells and its mechanism in vitro and in vivo. Methods The human OSCC cell lines Tca-8113 and the cisplatin-resistant cell line Tca-8113-CDDP were cultured with β-Ele or/and cisplatin. MTT assay was used to detect the cisplatin or β-Ele cytotoxicity and the cell viability. The cell cycles and cell apoptosis were detected by the flow cytometry. The expression of caspase-3, Bax, Bcl-2, STAT3, p-STAT3, JAK2, p-JAK2 were detected by western blot. The xenograft tumor model of OSCC was established in nude mice and treated with cisplatin and/or β-Ele. The volume and weight of the transplanted tumor was measured, and the expression of p-JAK2 and p-STAT3 in the xenograft tumor tissues were determined by immunohistochemistry and the cell apoptosis were detected by TUNEL assays.Results The combination of β-Ele and cisplatin significantly suppressed the cell proliferation, induced cell cycle arrest, promoted the apoptosis of Tca-8113-CDDP cells, and suppressed the activation of JAK2/STAT3 signaling pathway.The rescue experiments suggested that β-Ele enhanced cisplatin sensitivity via down-regulating JAK2/STAT3 signaling pathway. In vivo, β-Ele and cisplatin synergistically suppressed the tumor growth and induced apoptosis, and down-regulated the expression of p-JAK2 and p-STAT3. Conclusions β-Ele inhibits the cell viability and enhances the cisplatin sensitivity of OSCC by blocking the activation of JAK/STAT3 signaling pathway in vitro and in vivo, and the combination of β-Ele and cisplatin maybe a novel treatment for OSCC. |
