Pathology, research and practice · 2019
Parkin enhances sensitivity of paclitaxel to NPC by arresting cell cycle.
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Jiang Bo, Ni Haifeng, Zhou Zhen, Li Yong
Аннотация
OBJECT: Parkin has been reported as a tumor suppressor gene. The current research found that Parkin expresses abnormally in nasopharynx cancer (NPC).
MATERIALS AND METHODS: C666-1 and HONE1 NPC cell lines were performed to evaluate the effect of Parkin on cell cycle and apoptosis, the potential mechanisms of paclitaxel resistant based on its relationship with Parkin. Cell viability were determined by Cell counting kit-8 (CCK-8) and was further performed to explore the NPC cell sensitivity for paclitaxel. Cell cycle and cell apoptosis were used by flow cytometry. Corresponding proteins in the biological effects were detected by western blotting.
RESULTS: Overexpression of Parkin conspicuously enhanced paclitaxel sensitivity to NPC cells, whereas depleting of Parkin reduced paclitaxel sensitivity. In addition, overexpression of Parkin significantly delayed the cell cycle progression in G2/M phase. Paclitaxel is an anti-mitotic chemotherapeutic, and inhibition of Parkin reduces the effects of paclitaxel on mitosis.
CONCLUSIONS: Loss of Parkin inhibits the NPC cell sensitivity to paclitaxel. Upregulation of Parkin enhances the sensitivity of paclitaxel to NPC which indicates that Parkin can be a potential therapy target for NPC. Parkin may not only participate the paclitaxel resistance, but also exert synergistic effect with paclitaxel on NPC therapy. Thus Parkin may be a potential target for cancer therapy.
MATERIALS AND METHODS: C666-1 and HONE1 NPC cell lines were performed to evaluate the effect of Parkin on cell cycle and apoptosis, the potential mechanisms of paclitaxel resistant based on its relationship with Parkin. Cell viability were determined by Cell counting kit-8 (CCK-8) and was further performed to explore the NPC cell sensitivity for paclitaxel. Cell cycle and cell apoptosis were used by flow cytometry. Corresponding proteins in the biological effects were detected by western blotting.
RESULTS: Overexpression of Parkin conspicuously enhanced paclitaxel sensitivity to NPC cells, whereas depleting of Parkin reduced paclitaxel sensitivity. In addition, overexpression of Parkin significantly delayed the cell cycle progression in G2/M phase. Paclitaxel is an anti-mitotic chemotherapeutic, and inhibition of Parkin reduces the effects of paclitaxel on mitosis.
CONCLUSIONS: Loss of Parkin inhibits the NPC cell sensitivity to paclitaxel. Upregulation of Parkin enhances the sensitivity of paclitaxel to NPC which indicates that Parkin can be a potential therapy target for NPC. Parkin may not only participate the paclitaxel resistance, but also exert synergistic effect with paclitaxel on NPC therapy. Thus Parkin may be a potential target for cancer therapy.