Abstract
Breast cancer is the most common invasive malignancy. In 2020, the number of new cases of breast cancer worldwide has replaced lung cancer as the No.1 cancer in the global. Breast cancer is the leading cause of cancer death among women worldwide. Mammary tumorigenesis is severely linked to obesity, one potential connection is chemerin. Chemerin is a chemoattractant protein secreted by adipocytes, which contributes to the progression of breast cancer. Cell proliferation, migration, and invasion are cellular processes associated with various stages of metastasis. These processes are associated with mitogen-activated protein kinase (MAPK) signaling pathway. In this study, human breast cancer cell lines MCF-7 and MDA-MB-231were utilized to determine the effect of chemerin on cell proliferation, migration, and key proteins of MAPK signaling pathway. We found that chemerin promoted cell proliferation and migration in a concentration-dependent manner. Interestingly, these effects of chemerin were through promoting the proteins phosphorylation of ATF2 and ERK1/2 but not p38, in MAPK signaling pathway. Specific inhibitors of JNK and ERK1/2 pathway showed that the effect exerted by chemerin in cell proliferation and migration in breast cancer cells was dependent on these proteins. Our findings suggest that chemerin promotes the development of mammary cancer cells through JNK and ERK signaling pathways.
LDL and free fatty acids increase proliferation and migration of estrogen receptor negative (ER−) MDA‐MB‐231 breast cancer cells: involvement of ACAT1 and MAPK signaling