PCP4/PEP19 promotes migration, invasion and adhesion in human breast cancer MCF-7 and T47D cells
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Takuya Yoshimura1, Taiji Hamada2, Hiroshi Hijioka1, Masakazu Souda2, Kazuhito Hatanaka2, Takako Yoshioka3, Sohsuke Yamada2, Masato Tsutsui4, Yoshihisa Umekita5, Norifumi Nakamura1, Akihide Tanimoto2
1Department of Oral and Maxillofacial Surgery, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
2Department of Pathology, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan
3Department of Pathology, Children’s Cancer Center, National Center for Child Health and Development, Tokyo, Japan
4Department of Pharmacology, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan
5Division of Organ Pathology, Faculty of Medicine, Tottori University, Yonago, Japan
Akihide Tanimoto, email: email@example.com
Keywords: PCP4/PEP19, breast cancer, EMT, migration, invasion
Abbreviations: Purkinje cell protein 4/peptide 19, PCP4/PEP19; epithelial-mesenchymal transition, EMT
Received: September 02, 2015 Accepted: January 22, 2016 Published: February 20, 2016
Purkinje cell protein (PCP) 4/peptide (PEP) 19 is expressed in Purkinje cells where it has a calmodulin-binding, anti-apoptotic function. We recently demonstrated that PCP4/PEP19 is expressed and inhibit apoptosis in human breast cancer cell lines. In the present study we investigated the role of PCP4/PEP19 in cell morphology, adhesion, migration, and invasion in MCF-7 and T47D human breast cancer cell lines. Knockdown of PCP4/PEP19 reduced the formation of filopodia-like cytoplasmic structures and vinculin expression, and enhanced E-cadherin expression. Activities of migration, invasion, and cell adhesion were also decreased after the knockdown of PCP4/PEP19 in MCF-7 and T47D cells. These results suggested that PCP4/PEP19 promotes cancer cell adhesion, migration, and invasion and that PCP4/PEP19 may be a potential target for therapeutic agents in breast cancer treatment which act by inhibiting epithelial-mesenchymal transition and enhancing apoptotic cell death.
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