HIF-1α induced long noncoding RNA FOXD2-AS1 promotes the osteosarcoma through repressing p21
| Autor: | Yuxiang Kang, Gui-Shi Li, Yongcheng Hu, Zhi-Peng Ren, He-Jun Zhao, Yancheng Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
Cyclin-Dependent Kinase Inhibitor p21
Male 0301 basic medicine Mice Nude HIF-1α RM1-950 Biology medicine.disease_cause FOXD2-AS1 Epigenesis Genetic 03 medical and health sciences 0302 clinical medicine Transcription (biology) Cell Line Tumor Gene expression medicine Animals Humans Enhancer of Zeste Homolog 2 Protein EZH2 Transcription factor Pharmacology Gene knockdown Osteosarcoma Base Sequence Oncogene p21 Promoter General Medicine Hypoxia-Inducible Factor 1 alpha Subunit Long non-coding RNA Gene Expression Regulation Neoplastic Treatment Outcome 030104 developmental biology 030220 oncology & carcinogenesis Cancer research Female RNA Long Noncoding Therapeutics. Pharmacology Carcinogenesis |
| Zdroj: | Biomedicine & Pharmacotherapy, Vol 117, Iss, Pp-(2019) |
| ISSN: | 0753-3322 |
| Popis: | Emerging literature indicates the essential roles of long noncoding RNA (lncRNA) in the osteosarcoma (OS). However, the regulatory function and mechanism of FOXD2-AS1 in the OS is still elusive. In present research, the level of FOXD2-AS1 was significantly up-regulated in the OS tissue and cell lines compared to corresponding controls. The aberrant high-expression of FOXD2-AS1 indicated the poor clinical prognosis of OS patients. Transcription factor HIF-1α could bind with the promoter region of FOXD2-AS1 to activate the transcription in OS cells. Functionally, the knockdown of FOXD2-AS1 could repress the malignant biological properties of OS cells in vitro and vivo, including proliferation, invasion, apoptosis and tumor growth. Mechanistically, FOXD2-AS1 inhibited the expression of p21 via interacting with EZH2 to silence p21 gene expression. Overall, we conclude that FOXD2-AS1, induced by transcription factor HIF-1α, acts as an oncogene in the OS tumorigenesis and FOXD2-AS1 interacts with EZH2 to silence p21 protein. This finding could provide a novel insight and potential therapeutic target for the OS. |
| Databáze: | OpenAIRE |
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