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热疗可促进C6大鼠胶质瘤细胞凋亡并抑制其侵袭。

Hyperthermia promotes apoptosis and suppresses invasion in C6 rat glioma cells.

作者信息

Wang Dong-Chun, Zhang Yan, Chen Hai-Yan, Li Xiao-Li, Qin Li-Juan, Li Ya-Juan, Zhang Hong-Yi, Wang Shuo

机构信息

Tangshan Worker Hospital, Tangshan, China.

出版信息

Asian Pac J Cancer Prev. 2012;13(7):3239-45. doi: 10.7314/apjcp.2012.13.7.3239.

Abstract

Gliomas are a group of heterogeneous primary central nervous system tumors. Hyperthermia has proven to be a potential therapeutic tool for cancers in the clinic. However, the molecular mechanisms of hyperthermia remain unclear. The objective of this study was to investigate the effects of hyperthermia on the invasiveness in C6 glioma cells and related molecular pathways. Here our data show hyperthermia stimulated the release of tumor necrosis factor-alpha (TNF-α) and decreased C6 glioma cell migration and invasive capability at 30, 60, 120 and 180 min; with increased spontaneous apoptosis in C6 glioma cells at 120 min. We also found mitogen-activated protein kinase (P38 MAPK) protein expression to be increased and nuclear factor-kappa B (NF-κB) protein expression decreased. Based on the results, we conclude that hyperthermia alone reduced invasion of C6 glioma cells through stimulating TNF-α signaling to activate apoptosis, enhancing P38 MAPK expression and inhibiting the NF-κB pathway, a first report in C6 rat glioma cells.

摘要

胶质瘤是一组异质性原发性中枢神经系统肿瘤。在临床上,热疗已被证明是一种治疗癌症的潜在工具。然而,热疗的分子机制仍不清楚。本研究的目的是探讨热疗对C6胶质瘤细胞侵袭性及相关分子途径的影响。我们的数据显示,热疗在30、60、120和180分钟时刺激肿瘤坏死因子-α(TNF-α)的释放,降低C6胶质瘤细胞的迁移和侵袭能力;在120分钟时,C6胶质瘤细胞的自发凋亡增加。我们还发现丝裂原活化蛋白激酶(P38 MAPK)蛋白表达增加,核因子-κB(NF-κB)蛋白表达减少。基于这些结果,我们得出结论,单纯热疗通过刺激TNF-α信号激活凋亡、增强P38 MAPK表达和抑制NF-κB途径来降低C6胶质瘤细胞的侵袭,这在C6大鼠胶质瘤细胞中尚属首次报道。

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