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

Hyun-Joo Park | Zendy; Mi-Kyoung Kim | Zendy; KyuSil Choi | Zendy; JooWon Jeong | Zendy; SooKyung Bae | Zendy; Hyung Joon Kim | Zendy; MoonKyoung Bae | Zendy

Open Access

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

Author(s) -

Hyun-Joo Park,

Mi-Kyoung Kim,

KyuSil Choi,

JooWon Jeong,

SooKyung Bae,

Hyung Joon Kim,

MoonKyoung Bae

Publication year - 2016

Publication title -

international journal of oncology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.405

H-Index - 122

ISSN - 1019-6439

DOI - 10.3892/ijo.2016.3590

Subject(s) - epithelial–mesenchymal transition , autocrine signalling , cancer research , metastasis , breast cancer , downregulation and upregulation , vimentin , oncogene , cancer , biology , cancer cell , cell cycle , receptor , medicine , immunology , immunohistochemistry , biochemistry , gene

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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