Abstract
Ovarian cancer (OC) is the leading cause of death from gynecological cancer. In this study, we aimed to explore the role and potential mechanism of LIMD2 during the progression of OC. The expression of LIMD2 was analyzed by GEPIA (Gene Expression Profiling Interactive Analysis) database. Western blot and real-time PCR were applied to detect the gene expression of LIMD2 in OC cell lines. Cell counting kit-8 (CCK-8) assay, transwell, wound healing assays, and tumor xenograft experiments were used to evaluate the function of LIMD2 in vitro and vivo. Further, the LIMD2-associated pathways in OC were predicted by RNA-seq analysis, and the involvement of the corresponding cell signaling activities were confirmed by Western blot. We found that LIMD2 was high expressed in OC. Additionally, we found that silencing of LIMD2 inhibited OC cell proliferation in vitro and reduced the growth of its xenograft tumors. Moreover, knockdown of LIMD2 significantly decreased the migration of OC cells. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that pathways regulating extracellular matrix (ECM)-receptor interactions and focal adhesion signaling, were deregulated by LIMD2. Particularly, we confirmed that reducing LIMD2 could decrease the expression of Focal adhesion kinase (FAK) pathway related molecules. In conclusion, LIMD2 promotes the proliferation and invasion of ovarian cancer in vitro and in vivo, potentially through regulating the focal adhesion signaling pathway.