CRB3诱导乳腺癌他莫昔芬耐药细胞LCC2凋亡的机制研究

The mechanism of CRB3 induced apoptosis of tamoxifen resistant breast cancer LCC2 cell

目的:探讨细胞极性蛋白CRB3诱导乳腺癌他莫昔芬耐药细胞LCC2凋亡的作用机制。方法:运用免疫组织化学和WesternBlot技术分析CRB3在乳腺癌他莫昔芬耐药组织和细胞中的表达情况,流式技术和Western Blot观察CRB3对乳腺癌耐药细胞LCC2凋亡的影响及分子机制。结果:IHC结果证实,CRB3在乳腺癌他莫昔芬耐药组织中表达降低(P=0.004),Western Blot结果也显示CRB3在LCC2中表达较对照细胞MCF7表达降低;流式结果显示CRB3过表达引起LCC2的凋亡增加(P<0.05),Western Blot结果显示CRB3过表达引起LCC2的caspase3的活化增加,促凋亡因子Bax表达水平升高。抑凋亡因子Bcl2表达水平降低。结论:CRB3可通过激活caspase3途径诱导LCC2细胞的凋亡,以期成为乳腺癌他莫昔芬耐药预测和治疗的靶标。

Objective:To investigate the mechanism underlying CRB3 induction of apoptosis of tamoxifen resistant breast cancer cell LCC2.Methods:The CRB3 expressions in tamoxifen resistant breast cancer tissues and cells was detected by immunohistochemistry and Western Blot.The mechanism of CRB3 induction of apoptosis of tamoxifen resistant breast cancer cell LCC2 was analyzed by flow cytometry assay and Western Blot.Results:Immunohistochemistry indicted that CRB3 expression was lower in tamoxifen resistant and metastasis breast cancer than primary tumors ( P =0.004).Western Blot results showed that the expression of CRB3 in LCC2 cells was lower than control MCF7 cells.Flow cytometry assay results showed that CRB3 overexpression increased the apoptosis of LCC2 ( P <0.05).Western Blot results showed that CRB3 overexpression activated caspase 3,increased the apoptotic factor Bax,and decreased the apoptotic factor Bcl2.Conclusion:CRB3 induce the apoptosis of LCC2 cells,which can be used as an effective target for the prediction and treatment of tamoxifen resistance in breast cancers.