Triple-negative breast cancer (TNBC) is challenging to treat due to its aggressive nature. Its lack of hormone receptors renders conventional therapies less effective. This study assessed the efficacy of a novel compound, compound 2, in modulating TNBC cell behaviour. We used in vitro assays with MDA-MB-468 and MDA-MB-231 cell lines. Methods included annexin V apoptosis assay, flow cytometry for cell cycle and qRT-PCR for gene expression. Clonogenic, adhesion and wound healing assays were used for phenotypic characterization. Cytokine and chemokine levels in MDA-MB-468 cells were also measured using a Luminex assay. Compound 2 increased both early and late apoptosis in cancer cells, particularly MDA MB 468 cells. It also upregulated pro-apoptotic genes while downregulating anti-apoptotic genes. Additionally, it induced G1-phase arrest in MDA MB 468 cells with downregulation in Ki67 expression. Compound 2 also reduced cancer stem cell populations, suppressed colony formation, and impaired cell migration at IC50 concentrations. Significant changes in gene expression profiles for EMT-related genes were observed. Compound 2 decreased IL4 and IL8 levels and increased CCL2 and CXCL1. However, it did not significantly affect the levels of IL6, IL10, CXCL2, CCL5, TNF-α, IFN-γ, IL-1β, and IL2. Compound 2 thus exhibited a multifaceted anticancer profile, suggesting its potential in preventing cancer relapse and limiting cell proliferation which makes it a promising candidate for TNBC targeted therapy. This study lays the groundwork for further in vivo studies and potential clinical applications to explore full therapeutic potential of compound 2 in aggressive breast cancer types.
Tuah et al. (Fri,) studied this question.