Neuromedin B receptor antagonism inhibits migration, invasion, and epithelial-mesenchymal transition of breast cancer cells

  • Int J Oncol. 2016 Sep;49(3):934-42. doi: 10.3892/ijo.2016.3590.
Hyun-Joo Park  1 ,  Mi-Kyoung Kim  1 ,  Kyu-Sil Choi  2 ,  Joo-Won Jeong  3 ,  Soo-Kyung Bae  4 ,  Hyung Joon Kim  1 ,  Moon-Kyoung Bae  1
Affiliations
  • 1. Department of Oral Physiology, School of Dentistry, Pusan National University, Yangsan 626-870, Republic of Korea.
  • 2. Molecular and Cellular Imaging Center, Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul 136‑710, Republic of Korea.
  • 3. School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
  • 4. Department of Dental Pharmacology, BK21 PLUS Project, School of Dentistry, Pusan National University, Yangsan 626-870, Republic of Korea.
PMID: 27571778 DOI: 10.3892/ijo.2016.3590
Abstract

Neuromedin B (NMB) acts as an autocrine growth factor and a pro-angiogenic factor. Its receptor, NMB receptor (NMB-R), is overexpressed in solid tumors. In the present study, we showed that an NMB-R antagonist, PD168368, suppresses migration and invasion of the human breast Cancer cell line MDA-MB-231. In addition, PD168368 reduced epithelial-mesenchymal transition (EMT) of breast Cancer cells by E-cadherin upregulation and vimentin downregulation. Moreover, we found that PD168368 potently inhibits in vivo metastasis of breast Cancer. Taken together, these findings suggest that NMB-R antagonism may be an alternative approach to prevent breast Cancer metastasis, and targeting NMB-R may provide a novel therapeutic strategy for breast Cancer treatment.

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