CiRS-7 promotes growth and metastasis of esophageal squamous cell carcinoma via regulation of miR-7/HOXB13
Autor: | Weng-feng Wang, Shun Ke, Zhi-gang He, Xiao-jing Zou, Ming-hao Fang, Jun Lu, Fan-kai Meng, Rui-chao Li |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Male Cancer Research Esophageal Neoplasms Colorectal cancer Immunology Kaplan-Meier Estimate Disease-Free Survival Article Metastasis Pathogenesis 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine Downregulation and upregulation RNA interference Cell Movement Cell Line Tumor medicine Carcinoma Humans lcsh:QH573-671 Phosphorylation RNA Small Interfering Cell Proliferation Homeodomain Proteins lcsh:Cytology Cell growth business.industry Transcription Factor RelA Cancer Cell Biology RNA Circular Middle Aged medicine.disease Prognosis MicroRNAs 030104 developmental biology 030220 oncology & carcinogenesis Cancer research Carcinoma Squamous Cell RNA Female RNA Interference business Signal Transduction |
Zdroj: | Cell Death & Disease Cell Death and Disease, Vol 9, Iss 8, Pp 1-13 (2018) |
ISSN: | 2041-4889 |
Popis: | The circular RNA ciRS-7 has been reported to be involved in the pathogenesis of various tumors, including gastric and colorectal cancer. However, the role of ciRS-7 in esophageal squamous cell carcinoma (ESCC) remains unsolved. In this study, we found that the ciRS-7 expression was significantly upregulated in ESCC cancer tissues compared with matched normal tissues and associated with poor patient survival. Overexpression of ciRS-7 abrogated the tumor-suppressive roles of miR-7 including cell proliferation, migration and invasion in vitro as well as tumor growth and lung metastasis in vivo. Mechanistically, ciRS-7 functioned as the sponge of miR-7 and reactivated its downstream HOXB13-mediated NF-κB/p65 pathway. Conclusively, our findings demonstrate how ciRS-7 induces malignant progression of ESCC and that ciRS-7 may act as a novel prognostic marker and therapeutic target for this lethal disease. |
Databáze: | OpenAIRE |
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