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Molecules 2018, 23(1), 121; https://doi.org/10.3390/molecules23010121

VSP-17, a New PPARγ Agonist, Suppresses the Metastasis of Triple-Negative Breast Cancer via Upregulating the Expression of E-Cadherin

1
Guangxi Colleges and Universities Key Laboratory of Pharmacology, Guilin Medical University, 109 Huanchengbei Road Two, Guilin 541004, China
2
Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China
These authors equally contributed to this paper.
*
Authors to whom correspondence should be addressed.
Received: 20 December 2017 / Revised: 4 January 2018 / Accepted: 7 January 2018 / Published: 8 January 2018
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Abstract

Triple-negative breast cancer (TNBC), an aggressive subtype of breast cancer, shows higher metastases and relapse rates than other subtypes. The metastasis of TNBC is the main reason for the death of TNBC patients. Increasing evidence has shown that inhibiting the metastasis of TNBC is a good method for TNBC treatment. Here, VSP-17 was designed and synthesized as an agonist of PPARγ, evidenced by upregulating the expression of CD36 and increasing the activity of PPARγ reporter gene. VSP-17 obviously inhibited the migration and invasion process of MDA-MB-231 cells but showed little effect on the viability of MDA-MB-231 cells. Notably, VSP-17 could selectively promote the expression of E-cadherin without affecting the expression of BRMS1, CXCL12, MMP9, Orai1, Stim1, TGF-β, and VEGF. In addition, VSP-17 significantly suppressed the metastasis of liver and promoted the expression of E-cadherin in MDA-MB-231 xenograft model. In conclusion, VSP-17 inhibited the metastasis process of TNBC via upregulating the expression of E-cadherin. View Full-Text
Keywords: VSP-17; triple-negative breast cancer; metastasis; E-cadherin; PPARγ; agonist VSP-17; triple-negative breast cancer; metastasis; E-cadherin; PPARγ; agonist
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Wang, Y.; Zhu, M.; Yuan, B.; Zhang, K.; Zhong, M.; Yi, W.; Xu, X.; Duan, X. VSP-17, a New PPARγ Agonist, Suppresses the Metastasis of Triple-Negative Breast Cancer via Upregulating the Expression of E-Cadherin. Molecules 2018, 23, 121.

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