POTENT INDUCTION OF APOPTOSIS IN MCF-7 ER-POSITIVE BREAST CANCER CELLS BY CID-6861424 THROUGH INHIBITION OF AKT PROLIFERATION AND ERK SURVIVAL PATHWAYS

Abstract

Estrogen receptor-positive (ER-positive) breast cancer represents a significant subset of breast cancer cases, often characterized by resistance to conventional therapies. Targeting specific molecular pathways involved in cell proliferation and survival has emerged as a promising approach to overcoming this resistance. In this study, we explore the therapeutic potential of CID-6861424, a small molecule inhibitor, in inducing apoptosis in MCF-7 ER-positive breast cancer cells. Our research demonstrates that CID-6861424 exerts a potent anti-proliferative effect, primarily through the inhibition of the Akt and ERK signaling pathways, which are crucial for cell survival and proliferation in cancer cells.Upon treatment with CID-6861424, a significant reduction in cell viability was observed, accompanied by marked downregulation of phosphorylated Akt and ERK, indicating effective pathway inhibition. Flow cytometry analysis revealed an increase in apoptotic cell populations, which was further confirmed by the upregulation of apoptotic markers such as cleaved caspase-3 and PARP, along with the downregulation of the anti-apoptotic protein Bcl-2. These findings suggest that the induction of apoptosis by CID-6861424 is mediated through the disruption of the Akt and ERK pathways, leading to the activation of pro-apoptotic signals and inhibition of cell survival mechanisms. The results of this study highlight the potential of CID-6861424 as a novel therapeutic agent for ER-positive breast cancer. Its ability to target key signaling pathways involved in cancer cell survival positions it as a promising candidate for further development and clinical evaluation.