@article{oai:showa.repo.nii.ac.jp:00002953,
 author = {OKAZAKI, Keinosuke and SASAKI, Akiko and TSUNODA, Yuko and FURUYA, Kanji and TSUJI, Mayumi and UDAKA, Yuko and OYAMADA, Hideto and HOSONUMA, Masahiro and SHIRAKO, Haruna and YASUMOTO, Taro and KIUCHI, Yuji and SASAKI, Tadanori},
 issue = {3},
 journal = {The Showa University journal of medical sciences},
 month = {2018-09, 2019-08-05},
 note = {Triple-negative breast cancer （TNBC） accounts for 10-15％ of all breast cancer cases and shows a poor prognosis with 30％ distant metastasis. With few specific target molecules and ineffective hormonal and anti-HER2 treatment, an alternative therapeutic method for TNBC is urgently required. Recently, a non-taxane inhibitor of microtubule dynamics called eribulin was developed for breast cancer therapy. Eribulin induces irreversible mitotic mass formation in cancer cells during the G2-M phase, initiating apoptosis; however, the mechanism underlying this eribulin activity remains unclear. We reported previously that exposing non-basal-like （NBL） TNBC cells to eribulin increases miR-195 expression, which in turn decreases the expression of targeted Wnt3a. The present study sought to further clarify the mechanism of this antitumor effect by exploring how eribulin affects Wnt/β - catenin signaling based on miRNA expression changes in TNBC. In an NBL type of human breast cancer cell line （MDA-MB-231 cells）, we compared the expression levels of Wnt/β catenin signaling pathway proteins in cells exposed to an miR-195 mimic （cells transfected with miR-195 and in which Wnt3a expression was suppressed） and in cells exposed to eribulin. Expression levels of Wnt3a, β -catenin, and GSK-3β were measured by ELISA and observed by fluorescence immunostaining. Wnt3a and β -catenin expression was significantly lower and GSK-3β expression was significantly higher in the cells exposed to eribulin and transfected with miR-195 mimic than in the untreated controls, suggesting that eribulin inactivates the Wnt/β -catenin signaling pathway. Therefore, a novel antitumor mechanism of eribulin was determined, whereby eribulin induces high expression of miR-195 to inactivate the Wnt/β -catenin signaling pathway in NBL-type TNBC.},
 pages = {359--370},
 title = {Eribulin Treatment Induces High Expression of miR-195 and Inactivates the Wnt/β - catenin Signaling Pathway in Triple-negative Breast Cancer},
 volume = {30},
 year = {}
}