ArticlePharmacological reports : PR2025
MIM1 - a selective Mcl-1 protein inhibitor augments the proapoptotic activity of moxifloxacin toward MDA-MB-231 triple-negative breast cancer cells - a preliminary in vitro study.
Article in Pharmacological reports : PR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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5 authors.
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Abstract
backgroundTriple-negative breast cancer (TNBC) is characterized by high invasiveness, high metastatic potential, and poor prognosis. TNBC is not sensitive to endocrine therapy or HER2-targeted treatment, highlighting the need for the development of standardized TNBC treatment regimens. Thus, the development of new TNBC treatment strategies has become an urgent need. MIM1 - BH3 mimetic, which inhibits Mcl-1 antiapoptotic protein, may be an efficacious molecule able to induce apoptosis. Previously, we found that moxifloxacin (MOXI) can modulate the Mcl-1 protein expression. Therefore, in the current study, we assessed the impact of MIM1 and MOXI/MIM1 mixtures on the viability and apoptosis in MDA-MB-231 breast cancer cells.
methodsThe viability of cells was assessed by the WST-1 assay. The proapoptotic activity of the tested compounds was determined by cytometric technique.
resultsThe results showed that MIM1 exerted high cytotoxic and proapoptotic potential. In the case of two-component models, we have demonstrated that the use of MOXI and MIM1 mixtures resulted in a significant intensification of both cytotoxic and proapoptotic activity - shown as a modulatory effect on mitochondrial membrane potential, cell cycle distribution, or DNA fragmentation, toward MDA-MB-231 cells when compared with MIM1 or MOXI alone.
conclusionsWe have reported, for the first time, the high proapoptotic activity of MIM1 toward MDA-MB-231 cells pointing to the Mcl-1 protein as an important molecular target. Moreover, the observed potential synergistic mode of action (expressed as a significant enhancement of the induction of apoptosis process) detected for MOXI and MIM1 in the two-component model may provide a new direction for further in vitro and in vivo experiments concerning the role of Mcl-1 protein in the treatment of TNBC. CLINICAL TRIAL NUMBER: Not applicable.
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