Abstract

BackgroundOvarian cancer is a common malignancy of the female reproductive system, with one of the highest mortality rates among all malignant tumors. However, the pathogenesis of ovarian cancer has not been fully elucidated. This study investigated the role and molecular mechanism of LINC00641 in the development and progression of ovarian cancer.MethodsQuantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the expression level of LINC00641 in ovarian cancer tissue and adjacent normal tissue. Cell Counting Kit-8 (CCK-8), colony formation, and Transwell assays were used to detect the effects of LINC00641 overexpression on the proliferation and migration of ovarian cancer cells. Bioinformatics analysis and luciferase reporter gene assay were employed to detect the binding of LINC00641 to the downstream target molecule, microRNA-320a (miR-320a). Western blotting was used to determine the effect of miR-320a overexpression on the expression of proliferation-related proteins [Ki-67 and proliferating cell nuclear antigen (PCNA)] and invasion-related proteins (E-cadherin, N-cadherin, and vimentin) in overexpressed LINC00641 cells.ResultsqRT-PCR results showed that LINC00641 was under-expressed in ovarian cancer tissue compared to adjacent tissue. Cell function experiments showed that the overexpression of LINC00641 could significantly inhibit the proliferation and migration of ovarian cancer cells. The luciferase reporter gene assay showed that LINC00641 could bind to miR-320a, and the overexpression of LINC00641 could markedly inhibit the expression of miR-320a in ovarian cancer cells. Overexpression of miR-320a could significantly block the inhibitory effect of LINC00641 on the proliferation and migration of ovarian cancer cells.ConclusionsAs a tumor suppressor gene, LINC00641 can inhibit the proliferation and invasion of ovarian cancer cells by targeting miR-320a. The LINC00641/miR-320a axis may be a new target for the early diagnosis, treatment, or prognosis of ovarian cancer patients.

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