Long Non-Coding RNA Urothelial Carcinoma Associated 1 Promotes Proliferation, Migration and Invasion of Osteosarcoma Cells by Regulating microRNA-182
| Autor: | Xilong Gong, Yueshu Wang, Qiang Li, Wanying Xing |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Physiology Bone Neoplasms Tissue inhibitor of metallapeptidase 2 Biology lcsh:Physiology lcsh:Biochemistry 03 medical and health sciences Cell Movement Cell Line Tumor microRNA Humans lcsh:QD415-436 Neoplasm Invasiveness Viability assay Protein kinase B PI3K/AKT/mTOR pathway Cell Proliferation microRNA-182 NF-κB pathway Gene knockdown Osteosarcoma lcsh:QP1-981 Cell growth Long non-coding RNA urothelial carcinoma associated 1 Transfection Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Apoptosis Cancer research RNA Long Noncoding PI3K/AKT/GSK3β pathway |
| Zdroj: | Cellular Physiology and Biochemistry, Vol 51, Iss 3, Pp 1149-1163 (2018) |
| ISSN: | 1421-9778 |
| Popis: | Background/Aims: Previous studies demonstrated the oncogenic roles of lncRNA UCA1 in osteosarcoma. This study aimed to explore the internal molecular mechanism of UCA1 on promoting osteosarcoma cell proliferation, migration and invasion. Methods: qRT-PCR was conducted to measure the expression levels of UCA1, miR-182 and TIMP2. Cell transfection was used to change the expression levels of UCA1, miR-182 and TIMP2. Cell viability, migration, invasion and apoptosis were measured using CCK-8 assay, two-chamber migration (invasion) assay and Guava Nexin assay, respectively. The associations between UCA1, miR-182 and iASPP were analyzed by dual luciferase activity assay. The protein expression levels of key factors involved in cell apoptosis, PI3K/AKT/GSK3β pathway and NF-κB pathway, as well as p53, Rb, RECQ family and iASPP were evaluated by western blotting. Results: UCA1 was highly expressed in osteosarcoma MG63 and OS-732 cells. Knockdown of UCA1 inhibited OS-732 cell viability, migration and invasion, but promoted cell apoptosis. miR-182 was up-regulated in OS-732 cells after UCA1 knockdown and participated in the effects of UCA1 on OS-732 cells. TIMP2 was downstream factor of miR-182 and involved in the regulatory roles of miR-182 on OS-732 cell viability, migration, invasion, apoptosis, as well as PI3K/AKT/GSK3β and NF-κB pathways. UCA1 knockdown up-regulated p53, Rb and RECQL5 levels in OS-732 cells, while down-regulated the expression of iASPP. TGF-β or TNF-α treatment could enhance the expression of UCA1 in OS-732 cells. Conclusion: Our research verified that UCA1 exerted oncogenic roles in osteosarcoma cells by regulating miR-182 and TIMP2, as well as PI3K/AKT/GSK3β and NF-κB pathways. |
| Databáze: | OpenAIRE |
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