The Study On The Effect Of GLIPR1 On The Ovarian Cancer Cell Proliferation,Migration And Invasion And Its Related Mechanism

Background and purposeGLIPR1 was first discovered in human glioma which belongs to the CAP superfamily.Since the N-terminal of GLIPR1 contains a signal peptide and its C-terminal includes a transmembrane domain,these features indicate that GLIPR1 has functions like secreted or membrane protein.Studies have reported that the expression of GLIPR1 is up-regulated in glioma,Wilm’s tumor and melanoma,while it is significantly down-regulated in prostate cancer,bladder cancer and lung cancer.As a target gene of P53,the expression of GLIPR1 in various tumors is regulated by the methylation level of its promoter.In glioma and melanoma,epigenetic studies demonstrated that the hypomethylation of the GLIPR1 promoter region leads to upregulation of GLIPR1 expression.In prostate cancer and bladder cancer,the GLIPR1 promoter region is significantly hypermethylated and results in down-regulation of GLIPR1 expression.About the function of GLIPR1 in different tumors,it plays a pro-cancer role in glioma and melanoma,and can promote the growth,proliferation,migration and invasion of tumor cells.In prostate cancer and lung cancer,overexpression of GLIPR1 can augment the production of reactive oxygen species which in turn activate c-Jun-NH2 kinase signaling pathway and induce cell apoptosis.In summary,it can be known that the expression level and role of GLIPR1 gene vary greatly in different tumors.However,there are few studies about the expression of GLIPR1 in ovarian cancer.Although there was a study revealed that the expression of GLIPR1 is observably lower in malignant ovarian cancer tissues than normal ovarian tissues through sequencing analysis,no corresponding functional studies have been conducted on the specific role of GLIPR1 in ovarian cancer.This research aims to expound the expression level of GLIPR1 in ovarian cancer and explore the influence of GLIPR1 on the occurrence and evolution of ovarian cancer and related molecular mechanisms.MethodsFirst,the GEPIA database was utilized to investigate the correlation between GLIPR1 m RNA expression in ovarian cancer tissue and the outcome of ovarian cancer patients.Used QPCR and immunohistochemical to detect the expression and disposition of GLIPR1 in ovarian cancer.Transfected lentivirus with silenced and overexpressed GLIPR1 plasmids into corresponding high and low expression GLIPR1 human ovarian cancer cell lines,and utilized CCK8 proliferation assay,wound healing assay,migration chamber assay,invasion chamber assay and clone formation assay to detect what impacts of GLIPR1 on the biological behavior of ovarian cancer.Finally,detect the downstream pivotal factor of GLIPR1 that affect the biological behavior of ovarian cancer by western blot.ResultsThe expression level of GLIPR1 in ovarian cancer tissues had a positive correlativity with the poor outcome of patients.Furthermore,q PCR and immunohistochemical consequences had revealed that the expression level of GLIPR1 in ovarian cancer was higher than that in normal ovarian,and GLIPR1 protein was primarily distributed in the cytoplasm of carcinoma epithelial cells.CCK8 proliferation assay manifested that GLIPR1 facilitates the proliferation of ovarian cancer cells.The consequences of wound healing assay and migration chamber assay revealed that GLIPR1 accelerates migration of ovarian cancer cells.Invasion chamber assay manifested that GLIPR1 facilitates the invasion of ovarian cancer cells,and clone formation assay results revealed that GLIPR1 facilitates the clone formation of ovarian cancer cells.Finally,we evaluated by Western Blot that GLIPR1 could fortified the expression of MMP9.ConclusionsTo contrast normal ovarian tissue,the expression of GLIPR1 is enhanced in ovarian cancer tissue,and GLIPR1 is primarily expressed in the cytoplasm of ovarian epithelial cells.Moreover,the high expression of GLIPR1 in ovarian cancer forebodes a poor outcome.GLIPR1 may facilitates the proliferation,migration,invasion and colony formation of ovarian cancer cells by enhancing the expression of MMP9.