HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion
Tang Yiwei, Huang Hua, Guo Hui, Meng Mao, Long Xiang
Laboratory of Early Developmental and Injuries, West China Institutes for Woman and Children’s Health, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China (mainland)
Med Sci Monit 2015; 21:1856-1863
Available online: 2015-06-28
The aim of this study was to evaluate the effect of when silencing HOTAIR in ovarian cancer skov3 cells on proliferation, migration, and invasion, and to elucidate the mechanism by which this occurs.
MATERIAL AND METHODS: We detected the mRNA level of HOTAIR (HOX antisense intergenic RNA) and MAPK1 (mitogen-activated protein kinase 1) in ovarian cancer SKOV3, ES-2, OVCAR3, A2780, and COC1 cell lines. We detected the mRNA level of HOTAIR and MAPK1 in ovarian SKOV3 when transected with miR-1, miR-214-3p, or miR-330-5p. We detected the mRNA and protein level of MAPK1 when silencing HOTAIR. We detected the expression of HOTAIR when silencing MAPK1. Then we detected the proliferation, migration, and invasion in ovarian cancer skov3 after silencing HOTAIR or MAPK1.
RESULTS: The expression of HOTAIR and MAPK1 in ovarian SKOV3, ES-2, and OVCAR3 increased compared with A2780 and COC1 cells (P<0.05). The mRNA level of HOTAIR and MAPK1 in ovarian SKOV3 decreased when transected with miR-1, miR-214-3p, or miR-330-5p compared to negative control (p<0.05). The mRNA and protein level of MAPK1 was decreased when silencing HOTAIR and the mRNA level of HOTAIR was decreased when silencing MAPK1 (p<0.05). The proliferation, migration, and invasion was inhibited in ovarian SKOV3 after silencing HOTAIR or MAPK1 (p<0.05).
CONCLUSIONS: HOTAIR can promote proliferation, migration, and invasion in ovarian SKOV3 cells as a competing endogenous RNA.
Keywords: Cell Proliferation - physiology, Cell Line, Tumor, Gene Silencing, MicroRNAs - genetics, Mitogen-Activated Protein Kinase 1 - metabolism, Neoplasm Metastasis, Ovarian Neoplasms - pathology, RNA, Long Noncoding - physiology, RNA, Messenger - genetics