Long non-coding RNA HOXA11-AS functions as a competing endogenous RNA to regulate ROCK1 expression by sponging miR-124-3p in osteosarcoma
Autor: | Qingjiang Li, Xinli Zhan, Jinling Jia, Junlei Zhang, Mingxing Cui, Jingyu Wang |
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Rok vydání: | 2017 |
Předmět: |
0301 basic medicine
Adult Male Cell Survival Cell Biology Bioinformatics 03 medical and health sciences Young Adult 0302 clinical medicine medicine Gene silencing Humans ROCK1 RNA Antisense Pharmacology Homeodomain Proteins Osteosarcoma rho-Associated Kinases Cell growth Competing endogenous RNA General Medicine medicine.disease Long non-coding RNA Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology medicine.anatomical_structure Tumor progression 030220 oncology & carcinogenesis Cancer research Female RNA Long Noncoding |
Zdroj: | Biomedicinepharmacotherapy = Biomedecinepharmacotherapie. 92 |
ISSN: | 1950-6007 |
Popis: | Long non-coding RNAs (lncRNAs) have been strongly associated with various types of cancer. this study was to explore the critical role of lncRNA HOXA11-AS in osteosarcoma (OS) progression. Briefly, we should that the expression of HOXA11-AS was upregulated in OS tissues and cell lines. The high expression of HOXA11-AS was associated with advanced clinical stage, distant metastasis and poor overall survival of OS. In addition, We found that HOXA11-AS silencing suppressed OS cells proliferation, invasion and induced cell arrest in G0/G1 phase. Furthermore, our data showed that HOXA11-AS acts as an endogenous sponge by directly binding miR-124-3p, and decreasing the expression of miR-124-3p. Moreover, we found that HOXA11-AS may regulate tumor progression by affecting miR-124-3p targets, and ROCK1 expression. To conclude, our study helps to elucidate the effectiveness of HOXA11-AS promotion on OS cell proliferation and metastasis. A better understanding of interaction mechanism between HOXA11-AS-miR-124-3p-ROCK1 signaling axis may be a step forward in the development of new therapeutic strategies for the treatment of OS. |
Databáze: | OpenAIRE |
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