UM171 suppresses breast cancer progression by inducing KLF2

• DOI: 10.1007/s10549-024-07372-0
• Publication Date: 2024-06-14T05:02:33Z
• Authors: Xiaojuan Ran; Anling Hu; Yi Kuang; Chunlin Wang; Wuling Liu; Xiao Xiao; Eldad Zacksenhaus; Xiangdi Yu; Yaacov Ben-David
• Keywords: 0301 basic medicine; 03 medical and health sciences; Research

Abstract Purpose Breast cancer is the most frequent in women with significant death rate. Morbidity associated drug resistance and metastasis. Development of novel drugs unmet need. The aim this study to show potent anti-neoplastic activity UM171 compound on breast cells its mechanism action. Methods inhibitory effect several (BC) cell lines was examined using MTT colony-forming assays. Cell cycle apoptosis assays were utilized determine BC proliferation survival. Wound healing scratch transwell migration used examine culture. Xenograft mouse model 4T1 vivo. Q-RT-PCR western blotting expression level genes effected by UM171. Lentivirus-mediated shRNAs knockdown KLF2 cells. Results previously identified as a agonist human hematopoietic stem renewal inhibitor leukemia. In study, shown inhibit growth multiple UM171-mediated inhibition induction apoptosis, G2/M arrest, lower capacity, reduced motility. xenotransplantation triple-negative injected into syngeneic BALB/c mice, strongly inhibited tumor at comparable control paclitaxel. increased three PIM (PIM1-3) Moreover, induced suppressor gene P21 CIP 1 . Accordingly, lentivirus-mediated shRNA significantly attenuated As PIM1-3 act oncogenes are involved progression, these kinases likely impedes combination PAN-PIM LGH447 Conclusion These results suggested that progression part through activation P21. Combination offer therapy for aggressive forms cancer.