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28 June 2015 : Laboratory Research  

HOTAIR Interacting with MAPK1 Regulates Ovarian Cancer skov3 Cell Proliferation, Migration, and Invasion

Tang YiweiABCDEF, Huang HuaB, Guo HuiF, Meng MaoDE, Long XiangDEFG

DOI: 10.12659/MSM.893528

Med Sci Monit 2015; 21:1856-1863

Abstract

BACKGROUND: 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, Gene Silencing, MicroRNAs - genetics, Mitogen-Activated Protein Kinase 1 - metabolism, Neoplasm Metastasis, Ovarian Neoplasms - pathology, RNA, Long Noncoding - physiology, RNA, Messenger - genetics

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750