内质网应激对乳腺癌MCF-7细胞CCL5表达的影响
Endoplasmic Reticulum Stress-induced Overexpression of CCL5 in Human Breast Cancer Cell MCF-7
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摘要: 目的 探讨内质网应激水平与人乳腺癌MCF-7细胞CCL5表达之间的关系，明确CCL5与人乳腺癌MCF-7细胞增殖侵袭转移能力之间的关系。方法使用内质网应激诱导剂(Tuniamycin）和内质网应激抑制剂(4-PBA）分别处理人乳腺癌MCF-7细胞，24小时后提取细胞总蛋白。Western blot检测MCF-7细胞内质网应激水平及CCL5表达情况。MTT比色法，Transwell小室法检测细胞增殖和侵袭转移能力。结果内质网应激诱导剂处理组细胞内质网应激处于高水平，同时CCL5表达量增高；抑制剂组细胞内质网应激水平低，CCL5表达量也随之降低。并且诱导剂组肿瘤细胞增殖较抑制剂组活跃。升高的CCL5部分分泌到培养液中，影响细胞侵袭转移能力。结论内质网应激能够诱导人乳腺癌MCF-7细胞CCL5的表达；内源性CCL5能促进MCF-7细胞的增殖；外源性CCL5能促进MCF-7细胞侵袭转移。Abstract: Objective To discuss the relationship between ER stress and the expression of CCL5 in human breast cancer cell MCF-7 and identify the correlation between CCL5 and the proliferation and metastasis capacity of human breast cancer MCF-7 cells. Methods The ER stress and the expression of CCL5 in the tissue of human breast cancer and adjacent tissue were datected by Western blot.ER stress inducer Tuniamycin and ER stress inhibitor 4-PBA were used to MCF-7 cells respectively.Samples were collected the total cell protein after 24 hours treatment.Tthe ER stress and the expression of CCL5 in MCF-7 cells was analyzed by Westernblot.The proliferation and metastasis capacity of human breast cancer MCF-7 cells were measured by MTT colorimetry and transwell experiment respectively.ELISA was employed to detect the content of CCL5 in the culture medium. Results The ER stress and the expression of CCL5 in the tissue of human breast cancer were in higher level than that in adjacent tissue.The ER stress of the cells treated with ER stress inducer was in higher level and these cells expressed more CCL5.On the contrary，the ER stress of the cells treated with ER stress inhibitor was in lower level and these cells expressed less CCL5.In addition，the cells treated with ER stress inducer were more proliferative than the cells treated with ER stress inhibitor .CCL5 secreted to the culture medium could enhance the capacity of proliferation and metastasis of human breast cancer MCF-7 cells.ConclutionER stress can induce the endogenous expression of CCL5 in MCF-7 cells.Endogenous CCL5 can promote the proliferation of human breast cancer MCF-7 cells and extraneous CCL5 can promote the metastasis of MCF-7 cells.
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