Apelin-13 induces MCF-7 cell proliferation and invasion via phosphorylation of ERK1/2

Abstract

Apelin-13 is extensively expressed in various tissues, particularly breast tissue. Apelin-13 has been shown to promote tumor proliferation in various types of cancer, including hepatocellular, lung and ovarian cancer. However, the effect and molecular mechanism of apelin-13 in breast cancer cells remains unclear. The present study investigated the effect of apelin-13 on MCF-7. Therefore, cell proliferation was determined by MTT and flow cytometry analysis. The results revealed that apelin-13 markedly increased cell proliferation. Transwell assays demonstrated that apelin-13 increased MCF-7 cell invasion. Apelin-13 also markedly increased the expression of cyclin D1, extracellular matrix metalloproteinase-1 and amplified in breast cancer 1 (AIB1) in a dose-dependent manner by polymerase chain reaction assays. To study the molecular mechanism, cell proliferation, invasion and cyclin D1 were inhibited by pre-treatment with 10 μM of PD98059 (ERK1/2 inhibitor). Western blotting results suggested that apelin-13 significantly enhances the expression of p-ERK1/2 in a concentration-dependent manner. In conclusion, the results suggest that apelin-13 promoted MCF-7 cell proliferation and invasion via the ERK1/2/AIB1 signaling pathway.