Deng Xiaocong, Yang Xinming, Li Shisheng
Lin Chuang Er Bi Yan Hou Tou Jing Wai Ke Za Zhi. 2015 Jan;29(2):159-63.
Background: We detect the effects of Beclinl on paclitaxel-sensitivity in laryngeal carcinoma cell.
This study used Hep-2, Hep-2-pcDNA3. 1, Hep-2-Beclinl as invitro model. The effect of paclitaxel on the proliferation and cell apoptosis of laryngeal cancer cell lines was evaluated by MTT assay and flow cytometry. The protein expression level of Akt and p-Akt was detected by Western blot. Result: After treated by paclitaxel, the inhibition rate was significantly higher in Hep-2-Beclin cells than in Hep-2-pcDNA3. 1 cells and Hep-2 cells (P<. 05). After dealing with 10 tg/L paclitaxel, the apoptosis rate in Hep-2, Hep-2-pcDNA3. 1, Hep-2-Beclinl were (23. 75 ± 2 3. 77) %, (21. 25 ± 4. 92) %, (32. 50 ± 5. 97) %, respectively. After dealing with 20µg/L paclitaxel, the apoptosis rate in Hep-2, Hep-2-pcDNA3. 1, Hep-2-Beclinl were (38. 75 ± 4. 79) %, (38. 75±6. 55) %, (50. 00±7. 26) %, respectively. Paclitaxel-induced apoptosis was higher in Hep-2-Beclin cells than in Hep-2-pcDNA3. 1 cells and Hep-2 cells (P<. 05). The result of western blot showed that the protein expression level of p-Akt in Hep-2-Beclin cells was lower than in Hep-2-pcDNA3. 1 cells and Hep-2 cells (P<0. 05) and the protein expression level of Akt was similar in three cell lines (P>0. 05).
Beclinl enhances paclitaxel-sensitivity by inhibition of PI3K/Akt pathway.
背景：我们检测Beclin1对喉癌细胞中紫杉醇敏感性的影响。
本研究采用Hep-2、Hep-2-pcDNA3.1、Hep-2-Beclin1作为体外模型。通过MTT法和流式细胞术评估紫杉醇对喉癌细胞系增殖和细胞凋亡的影响。采用蛋白质免疫印迹法检测Akt和p-Akt的蛋白表达水平。结果：紫杉醇处理后，Hep-2-Beclin细胞的抑制率显著高于Hep-2-pcDNA3.1细胞和Hep-2细胞（P<0.05）。用10μg/L紫杉醇处理后，Hep-2、Hep-2-pcDNA3.1、Hep-2-Beclin1的凋亡率分别为（23.75±2.37）%、（21.25±4.92）%、（32.50±5.97）%。用20μg/L紫杉醇处理后，Hep-2、Hep-2-pcDNA3.1、Hep-2-Beclin1的凋亡率分别为（38.75±4.79）%、（38.75±6.55）%、（50.00±7.26）%。紫杉醇诱导的Hep-2-Beclin细胞凋亡高于Hep-2-pcDNA3.1细胞和Hep-2细胞（P<0.05）。蛋白质免疫印迹结果显示，Hep-2-Beclin细胞中p-Akt的蛋白表达水平低于Hep-2-pcDNA3.1细胞和Hep-2细胞（P<0.05），而三种细胞系中Akt的蛋白表达水平相似（P>0.05）。
Beclin1通过抑制PI3K/Akt通路增强紫杉醇敏感性。
