Endoplasmic Reticulum Stress-induced Overexpression of CCL5 in Human Breast Cancer Cell MCF-7

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.