التفاصيل البيبلوغرافية
العنوان:
Suppression of the Growth and Invasion of Human Head and Neck Squamous Cell Carcinomas via Regulating STAT3 Signaling and miR-21/β-catenin Axis with HJC0152
المؤلفون:
Zhaoqing Li , Sinan Wang , Na Ye , Jiabin Dong , Xuan Zhou , Minghui Zhao , Yansheng Wu , Yu Wang , Xudong Wang , Yu Ren , Xin Qu , Qiang Shen , Linhgping Kong , Kailiang Zhang , Yu Qiao , Chao Zhang , Shanshan Sun , Xiaofeng Yao , Wenyu Guo , Rui Jin , Lun Zhang , Haiying Chen , Chao Jing , Jia Zhou
سنة النشر:
2017
مصطلحات موضوعية:
0301 basic medicine , STAT3 Transcription Factor , Cancer Research , medicine.medical_specialty , Beta-catenin , Cell Survival , Cell , Antineoplastic Agents , Salicylanilides , Article , 03 medical and health sciences , Mice , 0302 clinical medicine , Internal medicine , Cell Line, Tumor , medicine , Animals , Humans , STAT3 , beta Catenin , Cell Proliferation , biology , Cell growth , Squamous Cell Carcinoma of Head and Neck , Cell cycle , Xenograft Model Antitumor Assays , Gene Expression Regulation, Neoplastic , MicroRNAs , 030104 developmental biology , medicine.anatomical_structure , Endocrinology , Oncology , Apoptosis , Head and Neck Neoplasms , 030220 oncology & carcinogenesis , Catenin , Cancer research , biology.protein , Carcinoma, Squamous Cell , Niclosamide , Signal transduction , Signal Transduction
الوصف:
Signal transducer and activator of transcription 3 (STAT3) is involved in the tumor growth and metastasis of human head and neck squamous cell carcinoma (HNSCC) and is therefore a target with therapeutic potential. In this study, we show that HJC0152, a recently developed anticancer agent and a STAT3 signaling inhibitor, exhibits promising antitumor effects against HNSCC both in vitro and in vivo via inactivating STAT3 and downstream miR-21/β-catenin axis. HJC0152 treatment efficiently suppressed HNSCC cell proliferation, arrested the cell cycle at the G0–G1 phase, induced apoptosis, and reduced cell invasion in both SCC25 and CAL27 cell lines. Moreover, HJC0152 inhibited nuclear translocation of phosphorylated STAT3 at Tyr705 and decreased VHL/β-catenin signaling activity via regulation of miR-21. Loss of function of VHL remarkably compromised the antitumor effect of HJC0152 in both cell lines. In our SCC25-derived orthotopic mouse models, HJC0152 treatment significantly abrogated STAT3/β-catenin expression in vivo, leading to a global decrease of tumor growth and invasion. With its favorable aqueous solubility and oral bioavailability, HJC0152 holds the potential to be translated into the clinic as a promising therapeutic strategy for patients with HNSCC. Mol Cancer Ther; 16(4); 578–90. ©2017 AACR.
اللغة:
English
الوصول الحر:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ce55a0ac3093153620dc592d3f16ec7fTest https://europepmc.org/articles/PMC5380531Test /
حقوق:
OPEN
رقم الانضمام:
edsair.doi.dedup.....ce55a0ac3093153620dc592d3f16ec7f
قاعدة البيانات:
OpenAIRE
