Long non-coding RNA CCAT2 acts as an oncogene in osteosarcoma through regulation of miR-200b/VEGF

• Published in: Artificial cells, nanomedicine, and biotechnology Vol. 47; no. 1; pp. 2994 - 3003
• Main Authors: Liu, Juntao, Kong, Dehai, Sun, Deping, Li, Jianmin
• Format: Journal Article
• Language: English
• Published: England 01.12.2019
• Subjects: AMP-Activated Protein Kinases - metabolism; Apoptosis - genetics; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Gene Expression Regulation, Neoplastic - genetics; Gene Knockdown Techniques; Humans; MicroRNAs - genetics; Neoplasm Invasiveness - genetics; Oncogenes - genetics; Osteosarcoma - genetics; Osteosarcoma - pathology; Phosphatidylinositol 3-Kinases - metabolism; Proto-Oncogene Proteins c-akt - metabolism; RNA, Long Noncoding - genetics; RNA, Long Noncoding - metabolism; Signal Transduction - genetics; Up-Regulation - genetics; Vascular Endothelial Growth Factor A - genetics; CCAT2; mobility; miR-200b; proliferation; Osteosarcoma; VEGF
• ISSN: 2169-141X
• DOI: 10.1080/21691401.2019.1640229

Colon cancer-associated transcript 2 (CCAT2) is a new lncRNA, which is closely associated with risk of several cancers. The aim of this study was to explore the regulatory mechanism of CCAT2 in osteosarcoma (OSA). Cells were transfected with si-CCAT2, microRNA (miR)-200b inhibitor and the corresponding controls. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was used to measure the expression of CCAT2 and miR-200b in OSA tissues and cell lines. CCK8 and bromodeoxyuridine (BrdU) were conducted to examine cell proliferation. Apoptosis was detected by PI/FITC-Annexin V combining with flow cytometric analysis. Migration and invasion were respectively measured through transwell chambers assays. Western blot was used to examine expressions of relative proteins. CCAT2 was highly expressed and miR-200b was lowly expressed in OSA tissues and cell lines. Knockdown of CCAT2 suppressed cell proliferation, migration and invasion but induced apoptosis and up-regulation of miR-200b. miR-200b inhibitor weakened the effect of si-CCAT2 on cell progression and cell mobility. Besides, knockdown of CCAT2 blocked the PI3K/Akt and AMPK pathways through up-regulating miR-200b. The CCAT2/miR-200b/vascular endothelial growth factor (VEGF) axis plays important regulating effect in OSA through the PI3K/Akt and AMPK pathways.