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In this study, we found that genetic alterations in several biological pathways, including ubiquitin protein ligase E3A (UBE3A) and its interacting genes such as HECT Type E3 INTERACTOR 4 (HIP4) and UBE3A autophagy, were common in these patients. Although these genes are already known to participate in ovarian cancer, the complex coordination and cross-talk among various pathways could provide novel insights into the pathogenesis, diagnosis, and treatment of ovarian cancer. During the metastatic spread of the tumor, tumor cells disseminate through the circulation and extravasate into distant tissues (6). The extracellular matrix (ECM) is comprised of a matrix of structural proteins and several secreted signaling factors. Among the signaling molecules in the ECM, some are known to be involved in cancer cell migration and invasion. The basement membrane, which is rich in several compounds, such as collagens, laminins, heparin sulfate glycoproteins, proteoglycans, and growth factors, is the first barrier for tumor spread. However, the ECM is not a barrier for tumor cells but can guide tumor cells into certain fates and become the target of tumor cell invasion. Altered ECM leads to differences in migration and invasion of tumor cells (7). These substances provide for the lifeline of tumor cells. In addition, ECM enables tumor cells to move and switch from one state to another, depending on the changes in the ECM, which alters expression of adhesion molecules and cell-matrix adhesion signaling pathways. The composition of the ECM molecules determines whether tumor cells adhere to the ECM and become motile, become stationary, or detach and invade metastases.

PCDH boxes, the cytoplasmic domain of protocadherins, are dispensable in epithelial cells. In neuronal cells, PCDH/N-cadherin complexes provide a growth-repressing signal. However, the role of PCDH20 in ovarian cancer is not known. Disruption of PCDH20 impairs cell growth and enhances apoptosis in multiple cancer cell lines, including ovarian cancer. d2c66b5586