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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。
Objective To investigate the relationship between the endoplasmic reticulum stress level and the expression of CCL5 in human breast cancer MCF-7 cells and to clarify the relationship between CCL5 and the proliferation, invasion and metastasis of human breast cancer MCF-7 cells. Methods Human breast cancer MCF-7 cells were treated with endoplasmic reticulum stress inhibitor (Tuniamycin) and endoplasmic reticulum stress inhibitor (4-PBA) respectively. Total cellular protein was extracted after 24 hours. Western blot detection of endoplasmic reticulum stress in MCF-7 cells and CCL5 expression. MTT colorimetric assay, Transwell chamber assay cell proliferation and invasion and metastasis. Results Endoplasmic reticulum stress inducing agent treatment group cells at high levels of endoplasmic reticulum stress, while CCL5 expression increased; inhibitor of endoplasmic reticulum stress level is low, CCL5 expression also decreases. The tumor cell proliferation in the inducer group was more active than that in the inhibitor group. Secreted CCL5 part of the secretion to the culture medium, affecting cell invasion and metastasis. Conclusion Endoplasmic reticulum stress can induce the expression of CCL5 in human breast cancer MCF-7 cells. Endogenous CCL5 can promote the proliferation of MCF-7 cells. Exogenous CCL5 can promote the invasion and metastasis of MCF-7 cells.