Abstract
Introduction: Breast cancer is the second most common cause of cancer-related deaths among women globally. Mitogen-activated protein kinases (MAPKs) are serine/threonine kinases with diverse cellular response functions. Additionally, p38 activation has been demonstrated in response to several external stimuli, including ultraviolet light, heat, osmotic shock, inflammatory cytokines, and growth factors. In this study, C₂₀H₁₃ClFN₃O compound’s cytotoxicity effect, apoptosis, and cell cycle arrest in MDA-MB-231 and MCF-7 cells were evaluated.
Objectives: To evaluate the potential of C₂₀H₁₃ClFN₃O compound as a p38 MAPK inhibitor for treating breast cancer.
Materials and Methods: This experimental study was conducted in-vitro to assess the anti-proliferative and apoptotic effects of C₂₀H₁₃ClFN₃O compounds on MDA-MB-231 and MCF-7 cells.
Results: The cytotoxicity assay showed that the half maximal inhibitory concentration of C₂₀H₁₃ClFN₃O in MCF-7 cells was 5.355 µg, and in MDA-MB-231 cells was 1.419 µg. In the FITC-annexin V apoptosis by flow cytometry in MCF-7 cells, the compound led to an increased early apoptotic by 70%. In contrast, in MDA-MB-231 cells, the compound led to a 23% increase in the early apoptotic effect. Furthermore, western blot results showed decreased p38 and NF-κB protein expression in both cell lines when treated with the compound.
Conclusion: In our study, the compound C₂₀H₁₃ClFN₃O that inhibits the p38 pathway shows promise as a new cancer treatment target. This study suggests that C₂₀H₁₃ClFN₃O could be a therapeutic target for breast cancer.