论文部分内容阅读
目的探索白细胞介素-13(interleukin-13,IL-13)对乳腺癌作用的分子机制。方法采用Transwell小室方法共培养人乳腺癌细胞与人成纤维细胞;RT-q PCR和Western blot检测IL-13对乳腺癌细胞抗凋亡因子B-cell lymphoma-2(Bcl-2)和TP53-induced glycolysis apoptosis regulator(TIGAR)表达的影响;Annexin V和CCK-8实验检测IL-13对乳腺癌细胞凋亡和增殖的影响。结果 IL-13上调了与人成纤维细胞CCC-ESF-1(ESF)共培养的人乳腺癌细胞BT-474的抗凋亡因子Bcl-2和TIGARm RNA和蛋白的表达。与其他各组比较,BT-474+ESF+IL-13组BT-474细胞的Bcl-2和TIGAR表达显著上调(P<0.05);加入IL-13可抑制BT-474细胞的凋亡,与BT-474+ESF共培养组比较,BT-474+ESF+IL-13共培养组的早期调亡的BT-474细胞下降了10.85倍;IL-13促进了BT-474细胞增殖,BT-474+ESF+IL-13组与各组比较,培养48 h、72 h、96 h和120 h后,BT-474细胞的增殖显著高于其它各组(P<0.05)。结论 IL-13可上调与人成纤维细胞共培养的人乳腺癌细胞BT-474抗凋亡因子Bcl-2和TIGAR的表达;IL-13对乳腺癌作用的分子机制涉及Bcl-2和TIGAR。
Objective To explore the molecular mechanism of interleukin-13 (IL-13) on breast cancer. Methods Human breast cancer cells and human fibroblasts were co-cultured with Transwell chamber method. The effects of IL-13 on the expression of Bcl-2 and TP53 in breast cancer cells were detected by RT-q PCR and Western blot. induced glycolysis apoptosis regulator (TIGAR). The effect of IL-13 on the apoptosis and proliferation of breast cancer cells was detected by Annexin V and CCK-8 assay. Results IL-13 up-regulated the expression of anti-apoptotic factors Bcl-2 and TIGARm RNA and protein of human breast cancer cell line BT-474 co-cultured with human fibroblast CCC-ESF-1 (ESF) Compared with other groups, the expression of Bcl-2 and TIGAR in BT-474 + ESF + IL-13 group was significantly increased (P <0.05); addition of IL-13 could inhibit the apoptosis of BT-474 cells and Compared with BT-474 + ESF co-culture group, BT-474 cells in BT-474 + ESF + IL-13 co-culture group decreased 10.85 times; BT- + ESF + IL-13 group, the proliferation of BT-474 cells was significantly higher than that of other groups (P <0.05) after cultured for 48 h, 72 h, 96 h and 120 h. Conclusion IL-13 can up-regulate the expression of anti-apoptotic factors Bcl-2 and TIGAR in human breast cancer cell line BT-474 which are co-cultured with human fibroblasts. The molecular mechanism of IL-13 on breast cancer involves Bcl-2 and TIGAR.