Nanomicellar TGX221 Inhibits N-Myc to Suppress Malignant Biological Behavior of Prostate Cancer Cells by Regulating MYC/Myc-Associated Factor X (MAX)

Abstract

Considering free amino N-terminal-myelocytomatosis viral oncogene homolog (N-Myc) as an important gene in prostate cancer (PC), we herein detected the impact of TGX-221 nanomicelles on N-Myc expression in PC cells. PC cells (LNCaP) were divided into blank group, empty vector group, N-Myc group and vector+N-Myc group, followed by analysis of myelocytomatosis viral oncogene homolog (MYC) and myc-associated factor (XMAX) expressions, cell proliferation, apoptosis and migration by CCK-8 method, flow cytometry and transwell experiment. Compared with blank group (4.95±0.67), N-Myc expression in the N-Myc group increased (6.25±0.78) but expressions in the empty vector (1.03±0.23) and vector+N-Myc groups (3.46±0.37) decreased significantly (P <0.05), with lowest expression in the empty vector group (P <0.05). Cell proliferation and migration in the N-Myc group increased within 96 h of transfection, but decreased in the empty vector and vector+N-Myc groups (P <0.05), and TGX-221-loaded N-Myc obtained the lowest proliferation and migration (P <0.05). N-Myc transfection decreased apoptosis, and nanomicellar TGX221 or N-Myc-loaded vector resulted in increased apoptotic cells (P < 0.05), with highest apoptosis in the vector+N-Myc group. Moreover, the presence of nanomicellar TGX221 reversed their expression with lowest expression in the vector+N-Myc group, as transfection with N-Myc increased MYC/MAX mRNA expression. TGX-221 nanomicelles inhibited N-Myc and MYC/MAX expression, thereby suppressing proliferation and migration of PC cells, and inducing cell apoptosis.