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- Title
HJC0152, a novel STAT3 inhibitor with promising anti-tumor effect in gastric cancer.
- Authors
Jiang, Xiaoxia; Wu, Mengjie; Xu, Zhenzhen; Wang, Haohao; Wang, Haiyong; Yu, Xiongfei; Li, Zhongqi; Teng, Lisong
- Abstract
Background: Aberrant activation of the signal transducer and activator of transcription 3 (STAT3) is frequently seen in patients with gastric cancer (GC), and is generally associated with worse prognosis. HJC0152, a novel STAT3 inhibitor, has shown significant anti-tumor effects in several cancers, although its role in GC remains to be clarified. Methods: The effect of HJC0152 on STAT3 signaling pathway and the biological behaviors of GC cells were evaluated through in vitro and/or in vivo experiments. Meanwhile, RNA sequence analysis was used to further explore its potential anti-tumor mechanisms. Results: HJC0152 inhibited the expression of activated STAT3 and its downstream target genes (c-Myc and clyclinD1) in GC cells, and restrained tumor growth in vivo. HJC0152 treatment induced apoptosis in the STAT3 hyper-activated AGS and MKN45 cell lines, along with down-regulation of survivin and Mcl1, and up-regulation of cleaved-poly(ADP-ribose) polymerase. Moreover, HJC0152 markedly inhibited migration and invasion of these cells. Finally, RNA sequence analysis and protein expression analyses showed that in addition to STAT3 suppression, HJC0152 also exerts its anti-tumor effects at least partly via the mitogen-activated protein kinases pathway. Conclusion: Our findings highlight that HJC0152 is a promising therapeutic agent for GC.
- Subjects
MITOGEN-activated protein kinases; CELL migration; RNA sequencing; PROTEIN expression; TUMOR growth
- Publication
Cancer Management & Research, 2018, Vol 10, p6857
- ISSN
1179-1322
- Publication type
Article
- DOI
10.2147/CMAR.S188364