Open Access

ARTICLE

A novel isoxazole compound CM2-II-173 inhibits the invasive phenotype of triple-negative breast cancer cells

EUN SOOK KIM¹, SANGHEE KIM², AREE MOON^1,*

1 Duksung Innovative Drug Center, College of Pharmacy, Duksung Women’s University, Seoul, 03169, Korea
2 College of Pharmacy, Seoul National University, Seoul, 08826, Korea

* Corresponding Author: AREE MOON. Email:

Oncology Research 2023, 31(6), 867-875. https://doi.org/10.32604/or.2023.030411

Received 04 April 2023; Accepted 11 July 2023; Issue published 15 September 2023

Abstract

Invasion and metastasis are important hallmarks of breast cancer and are the leading cause of patient mortality. Triple-negative breast cancer (TNBC) is an aggressive type of breast cancer characterized by a poor prognosis and a lack of effective targeted therapies. The present study investigated the inhibitory effect of a novel FTY720 derivative on the invasive phenotype of TNBC cells. Here, we showed that a novel compound with an isoxazole ring, 4-(3-Decylisoxazol-5-yl)-1-hydroxy-2-(hydroxymethyl)butan-2-aminium chloride (CM2-II-173), significantly inhibited invasiveness of MDA-MB-231 TNBC cells. Expression of matrix metalloproteinase (MMP)-9 and invasiveness of MCF10A normal breast cells induced by sphingosine-1-phosphate (S1P) were reduced by CM2-II-173 treatment. Activations of pMEK1, pAkt, pERK, and p38 MAPK by S1P were inhibited by treatment with CM2-II-173. Proliferation and anchorage-independent growth of MDA-MB-231 TNBC cells were significantly decreased by CM2-II-173. CM2-II-173 efficiently induced apoptosis in MDA-MB-231 TNBC cells. CM2-II-173 significantly inhibited invasive phenotypes of breast, liver, prostate, and ovarian cancer cells. CM2-II-173 exhibited a more potent effect on the invasiveness of MDA-MB-231 TNBC cells compared to FTY720. Taken together, this study demonstrated that CM2-II-173 has the potential to be a lead compound that can inhibit cancer progression of not only TNBC cells, but also of liver, prostate, and ovarian cancer cells.

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