Anticancer effects and underlying mechanisms of HJC0152, a small-molecule STAT3 in-hibitor, on tumor invasion and migration in human head and neck squamous cell carci-noma
10.3969/j.issn.1000-8179.2017.17.454
- VernacularTitle:STAT3小分子抑制剂HJC0152抑制人头颈部鳞癌细胞株侵袭迁移能力的研究
- Author:
LI ZHAOQING
1
;
WANG YU
;
QIAO YU
;
WU CHUANQIANG
;
ZHAO MINGHUI
;
SUN SHANSHAN
;
ZHANG LUN
Author Information
1. 天津医科大学肿瘤医院颌面耳鼻喉科
- Keywords:
small molecular inhibitor;
human head and neck squamous cell carcinoma (HNSCC);
neoplasm invasiveness;
epithelial–mesenchymal transition (EMT);
STAT3 transcription factor
- From:
Chinese Journal of Clinical Oncology
2017;44(17):841-845
- CountryChina
- Language:Chinese
-
Abstract:
Objective:This study aims to explore the anticancer effects and potential mechanisms of HJC0152, a novel STAT3 inhibitor, on the invasion and migration capacities of human head and neck squamous cell carcinoma (HNSCC) cell lines in vitro. Methods:Cells were divided into two groups, the dimethyl sulfoxide (DMSO) group and the HJC0152 group in which HNSCC cell lines UM-1 and SCC-15 were treated with DMSO or HJC0152 for 24 h. The total expression levels of STAT3, p-STAT3 (Tyr705/Ser727), MMP-2/9, N/E-cadherin, TWIST1, and vimentin;and the cytoplasm and nuclear expression levels of STAT3 and p-STAT3 (Tyr705/Ser727) were detected by Western blot assay. Wound healing and Transwell assays were employed to detect the invasion and migration abilities of the UM-1 and SCC-15 cells. The expression and location of N/E-cadherin were visualized by immunofluorescence staining. Results:Western blot indicated that the total expression of p-STAT3 (Tyr705), MMP-2/9, N-cadherin, TWIST1, and vimentin were significantly declined and that E-cadherin was remarkably elevated in the HJC0152 group cells compared with that of the DMSO group, with no difference in STAT3 or p-STAT3 (Ser727). Cytoplasm and nuclear STAT3 (Tyr705) were also inhibited by HJC0152. Wound healing and Transwel assays indicated that tumor invasion and migration capacities were impressively attenuated in the HJC0152 group cells compared to that of the DMSO group. Conclusion:HJC0152 suppresses the phosphorylation of STAT3 at Tyr705 in the HNSCC cell lines, leading to impair transcription activity, deplete expression levels of target genes, and subsequently inhibit migration and invasion capabilities of HNSCC.
