Up-regulation of long intergenic noncoding RNA 01296 in ovarian cancer impacts invasion,apoptosis and cell cycle distribution via regulating EMT |
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| Institution: | 1. Department of Gynecology, Qilu Hospital of Shandong University, Jinan 250012, Shandong, PR China;2. Department of Gynecology, The Second Hospital of Shandong University, Jinan 250033, Shandong, PR China;1. Center for Interdisciplinary Research, Tohoku University, Sendai 980-8578, Japan;2. Department of Project Programs, Tohoku University, Sendai 980-8575, Japan;3. Department of Molecular Immunology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai 980-8575, Japan;4. International Advanced Research and Education Organization, Tohoku University, Sendai 980-8578, Japan;5. Graduate School of Medicine, Tohoku University, Sendai 980-8575, Japan |
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| Abstract: | BackgroundRecently, long intergenic non-coding RNA 01296 (LINC01296) has been demonstrated to regulate the initiation and progression of several cancers, but the functions of LINC01296 in ovarian cancer still remain unclear. The objective of our study was to determine the expression, biological roles, and clinical significance of LINC01296 in ovarian cancer.MethodsLINC01296 expression was measured in ovarian cancer tissues or cell lines. Next, the relationships between LINC01296 levels and the clinical factors of ovarian cancer, such as progression-free survival and overall survival were analyzed. Additionally, cell proliferation, migration and invasion capacities, apoptosis, cell cycle distribution were investigated after silencing of LINC01296. To confirm whether LINC01296 mediates EMT initiation in ovarian cancer cells, the effect of LINC01296 silence on E-cadherin, N-cadherin and vimentin was assessed in SKOV3 and OVCAR3 cells.ResultsWe found that LINC01296 was over-expressed in ovarian cancer tissues and cell lines, when comparing with adjacent normal tissue samples and normal cells. Higher LINC01296 expression was significantly correlated with shorter progression-free survival and overall survival. For the functional experiments, knockdown of LINC01296 suppressed cell proliferation, inhibited colony formation ability, abrogated cell migration and invasion potential, and enhanced cell apoptosis. Cell cycle analysis suggested that LINC01296 positively regulated cell cycle progression in ovarian cancer cells. Moreover, western blotting analysis displayed that knockdown of LINC01296 significantly increased E-cadherin, but reduced N-cadherin and vimentin expressions in SKOV3 and OVCAR3 cells, compared with no-transfection cells.ConclusionsLINC01296 plays an important role in promoting the progression of ovarian cancer. Over-expression of LINC01296 might function as an indicator for diagnosis and prognosis of ovarian cancer patients. |
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