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目的:观察姜黄素对鼻咽癌细胞株C666-1增殖及凋亡的影响,探讨其可能的作用机制。方法:0、10、25、50及100μmol/L姜黄素作用24 h或50μmol/L姜黄素不同时间(0、6、12及24 h)后,CCK-8法检测C666-1细胞的增殖情况,TUNEL法检测细胞凋亡,Western blotting检测不同浓度姜黄素作用24 h后细胞内AMPK、S6K1及S6蛋白磷酸化情况。结果:与0μmol/L组比,50、100μmol/L姜黄素作用24 h后,对C666-1细胞增殖的抑制作用显著增强[(38.33±6.53)%、(21.14±5.36)%vs(100±0.00)%,均P<0.05];50μmol/L姜黄素作用6、12、24 h后,对C666-1细胞增殖的抑制作用显著增强[(49.6±5.67)%、(47.7±6.65)%、(46.86±9.4)%vs(100±0.00)%,均P<0.05]。50、100μmol/L姜黄素作用后细胞的凋亡率显著增加[(43±12.53)%、(48±8.54)%vs(2.87±1.03)%,均P<0.05],50μmol/L姜黄素作用12、24 h后,细胞凋亡率随作用时间延长而增加[(35.33±5.86)%、(47.33±13.01)%vs(4.33±3.21)%,均P<0.05]。50、100μmol/L姜黄素可促进细胞内AMPK磷酸化,抑制其下游mTOR信号通路中S6K及S6蛋白的磷酸化活化[(3.87±1.38)、(0.19±0.16)、(0.39±0.24)vs 1;(4.34±1.34)、(0.059±0.043)、(0.11±0.095)vs 1,均P<0.05]。结论:姜黄素可显著抑制鼻咽癌C666-1细胞增殖和诱导细胞凋亡,其机制可能与影响AMPK、S6K1及S6蛋白磷酸化有关。
Objective: To observe the effect of curcumin on proliferation and apoptosis of nasopharyngeal carcinoma cell line C666-1 and to explore its possible mechanism. Methods: The proliferation of C666-1 cells was detected by CCK-8 after treated with curcumin at 0, 10, 25, 50 and 100 μmol / L for 24 h or 50 μmol / L curcumin at various times (0, 6, 12 and 24 h) The apoptosis of cells was detected by TUNEL method. The phosphorylation of AMPK, S6K1 and S6 protein was detected by Western blotting after 24 h treatment with different concentrations of curcumin. Results: Compared with 0μmol / L group, the inhibitory effect of curcumin at 50 and 100μmol / L for 24 h on C666-1 cells was significantly enhanced (38.33 ± 6.53% vs 21.14 ± 5.36% vs (100 ± (49.6 ± 5.67)%, (47.7 ± 6.65)%, respectively. The inhibitory effect of curcumin on the proliferation of C666-1 cells was significantly enhanced after treated with 50 μmol / L curcumin for 6, 12 and 24 h (46.86 ± 9.4)% vs (100 ± 0.00)% respectively, all P <0.05]. The apoptosis rate of cells treated with 50,100μmol / L curcumin was significantly higher than that of the control group ([(43 ± 12.53)% vs (48 ± 8.54)% vs (2.87 ± 1.03)%, P <0.05] After 12 and 24 h, the apoptotic rate increased with the time prolonging [(35.33 ± 5.86)% and (47.33 ± 13.01)% vs (4.33 ± 3.21)%, both P <0.05]. Curcumin at 50 and 100μmol / L increased phosphorylation of AMPK and inhibited phosphorylation of S6K and S6 protein in downstream mTOR signaling pathway [(3.87 ± 1.38), (0.19 ± 0.16), (0.39 ± 0.24) vs 1 ; (4.34 ± 1.34), (0.059 ± 0.043), (0.11 ± 0.095) vs 1, all P <0.05]. CONCLUSION: Curcumin can significantly inhibit the proliferation and induce the apoptosis of C666-1 cells. The mechanism may be related to the phosphorylation of AMPK, S6K1 and S6.