Takayuki Iwamoto
   Department   Kawasaki Medical School  Kawasaki Medical School, Department of Breast and Thyroid Surgery,
   Position   Assistant Professor
Article types 原著
Language English
Peer review Peer reviewed
Title CSF-1/CSF-1R axis is associated with epithelial/mesenchymal hybrid phenotype in epithelial-like inflammatory breast cancer.
Journal Formal name：Scientific reports
Abbreviation：Sci Rep
ISSN code：20452322/20452322
Domestic / ForeginForegin
Volume, Issue, Page 8(1),pp.9427
Author and coauthor Kazuharu Kai, Takayuki Iwamoto, Dongwei Zhang, Li Shen, Yuko Takahashi, Arvind Rao, Alastair Thompson, Subrata Sen, Naoto T Ueno
Authorship 2nd author
Publication date 2018/06
Summary Inflammatory breast cancer (IBC) is a rare subtype of breast cancer, accounting for 8-10% of breast cancer-associated deaths in the US. Clinical hallmarks of IBC include tumor emboli in lymphatic vessels and E-cadherin overexpression, which supports a type of metastasis referred to as cell cluster-based metastasis, prevalent in IBC. In contrast, we previously reported epithelial-to-mesenchymal transition (EMT)-based progression of IBC, utilizing in vivo xenografts and in vitro Matrigel culture models. To address these two contradictory concepts of IBC metastasis, we used Matrigel culture to induce EMT in a panel of IBC cells. Results revealed Matrigel culture induced vimentin expression in SUM149 and SUM190 IBC cells at the transcriptional and protein levels while maintaining the expression of E-cadherin, a phenomenon referred to as partial EMT. Transcriptional profiling revealed that expression of colony-stimulating factor 1 (CSF-1) was induced in Matrigel culture. When the receptor tyrosine kinase of CSF-1 (CSF-1R) was inhibited by CSF-1R inhibitor BLZ945, the partial EMT was reversed in a dose-dependent manner, indicating that the CSF-1/CSF-1R axis plays a key role in controlling partial EMT. This observation may help reconcile the two contradictory theories of IBC metastasis, EMT vs cell cluster-based metastasis.
DOI 10.1038/s41598-018-27409-x
PMID 29930294