细胞缝隙连接对乳腺癌细胞紫杉醇敏感性的影响  

Effect of Gap Junction on the Sensitivity of Breast Cancer Cells to Paclitaxel

作　　者：李夏蔚 朱颖[1] 原野[1] 许亚[1] 陈文林[1] Li Xiawei;Zhu Ying;Yuan Ye;Xu Ya;Chen Wenlin(Xuzhou Central Hospital, Xuzhou 221000, China)

机构地区：[1]徐州市中心医院,徐州221000

出　　处：《中国药事》2018年第6期753-756,共4页Chinese Pharmaceutical Affairs

摘　　要：目的:探讨细胞缝隙连接对乳腺癌细胞紫杉醇敏感性的影响。方法:以乳腺癌T47D细胞为研究对象,采用CCK8法检测细胞毒性。结果:紫杉醇(TAX)的细胞毒性有细胞密度依赖性,与低密度相比,细胞在高密度时的毒性显著增加。这说明,细胞在高密度有缝隙连接(Gap Junction,GJ)形成的情况下,TAX的细胞毒性显著增加。此外,细胞在高密度的情况下,分别采用维甲酸(RA)和甘草次酸(18-α-GA)增强或抑制GJ功能,结果发现,RA组的TAX细胞毒性显著高于正常组,相反,给予18-α-GA抑制GJ功能后,TAX的细胞毒性显著降低。结论:增强GJ功能可显著提高乳腺癌细胞对TAX的敏感性。GJ可能是提高TAX对乳腺癌疗效的新靶点。Objective： To investigate the effect of gap junction on the sensitivity of breast cancer cells to Paclitaxel（TAX）. Methods： Breast cancer T47 D cells were used as objects and CCK8 assay was used to detect cytotoxicity. Results： The cytotoxicity of TAX was cell density dependent and the toxicity of cells at high densities has significantly increased compared to that at low density, indicating that the cell cytotoxicity of TAX significantly increased under the condition of high density and gap junction（GJ） formation. In addition, in the case of high density of cells, retinoic acid（RA） and glycyrrhetinic acid（18-α-GA） were used to enhance or inhibit GJ function respectively. The results showed that TAX cytotoxicity of RA group was significantly higher than that of the normal group, while the TAX cytotoxicity of 18-α-GA group reduced significantly. Conclusion： Enhancing GJ function can significantly improve the sensitivity of breast cancer cells to TAX. GJ may be a novel target spot to improve the efficacy of TAX in breast cancer.

关 键 词：细胞缝隙连接 紫杉醇 细胞毒性 

分 类 号：R979.1[医药卫生—药品] R737.9[医药卫生—药学]