UNBS5162 inhibits proliferation of human melanoma cells by inducing apoptosis via the PI3K/Akt pathway

作者：Shi, Xueli; Yang, Liu; Xie, Jun; Zhao, Yumei; Cong, Junzi; Li, Zhiping; Li, Haiyan; Cheng, Xianzhi; Fan, Jinghui^*

来源：Molecular Medicine Reports, 2018, 18(3): 3382-3388.

DOI：10.3892/mmr.2018.9321

• melanoma
• apoptosis
• naphthalimides
• signaling pathway

UNBS5162, a novel naphthalimide, is generated by UNBS3157 hydrolysis in physiological saline. In the present study, the effects of UNBS5162 on M14 human melanoma cells were evaluated by Cell Counting Kit-8 and transwell assays, as well as western blotting. The underlying mechanism of apoptosis induced by UNBS5162 was investigated. The results demonstrated that proliferation of UNBS5162-treated M14 melanoma cells was markedly inhibited in a time-dependent manner. The flow cytometry results indicated a markedly increased apoptosis rate in the experimental group compared with in the control group (23.8 +/- 0.4 vs. 7.62 +/- 0.5%). Microscopy analysis revealed that the invasive and migratory abilities of UNBS5162-treated M14 cells were markedly suppressed. Furthermore, UNBS5162 treatment led to decreased expression of the anti-apoptotic protein B-cell lymphoma 2, but increased expression of the pro-apoptotic proteins Bcl-2-associated X protein and caspase-3. In addition, the expression of several key proteins involved in the phosphatidylinositol-4,5-bisphosphate 3-kinaselprotein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway was altered in M14 cells treated with UNBS5162. Based on these results, it may be hypothesized that UNBS5162 suppresses the proliferation of M14 cells by inducing apoptosis via inhibition of key proteins in the PI3K/Akt/mTOR signaling pathway.

• 出版日期2018-9
• 单位牡丹江医学院