Juntao Liu1,2, Dehai Kong3, Deping Sun2, Jianmin Li1. 1. a Department of Orthopedics, Qilu Hospital of Shandong University , Jinan , PR China. 2. b Department of Orthopedic Trauma, Yantai Affiliated Hospital of Binzhou Medical University , Yantai , PR China. 3. c Department of Foot and Ankle Surgery, Binzhou Medical University Hospital , Binzhou , PR China.
Abstract
Background/aim: 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). Methods: 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. Results: 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. Conclusions: The CCAT2/miR-200b/vascular endothelial growth factor (VEGF) axis plays important regulating effect in OSA through the PI3K/Akt and AMPK pathways.
Background/aim: 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). Methods: 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. Results: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. Conclusions: The CCAT2/miR-200b/vascular endothelial growth factor (VEGF) axis plays important regulating effect in OSA through the PI3K/Akt and AMPK pathways.