title: 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 (ERK(1/2) inhibitor). Western blotting results suggested that apelin‑13 significantly enhances the expression of p‑ERK(1/2) 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.
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Xuewei
authors.initials: X
authors.lastname: Peng
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Fengyu
authors.initials: F
authors.lastname: Li
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Ping
authors.initials: P
authors.lastname: Wang
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Shengnan
authors.initials: S
authors.lastname: Jia
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Lili
authors.initials: L
authors.lastname: Sun
authors.affiliation: School of Life Sciences, Northeast Normal University, Changchun, Jilin 130024, P.R. China.
authors.forename: Hongliang
authors.initials: H
authors.lastname: Huo
mesh_terms: D001940:Breast / Q000378:metabolism / Q000473:pathology*; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology*; D049109:Cell Proliferation; D019938:Cyclin D1 / Q000235:genetics; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism*; D020935:MAP Kinase Signaling System; D061986:MCF-7 Cells; D020781:Matrix Metalloproteinase 1 / Q000235:genetics; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009361:Neoplasm Invasiveness / Q000473:pathology; D056921:Nuclear Receptor Coactivator 3 / Q000235:genetics; D010766:Phosphorylation
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; C495199:apelin-13 peptide; D019938:Cyclin D1; C538866:NCOA3 protein, human; D056921:Nuclear Receptor Coactivator 3; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020781:Matrix Metalloproteinase 1