Abstract:
Ovarian carcinoma is the second most leading cause of deaths among female
reproductive system malignant tumors. Serous epithelial carcinomas have a poor
treatment rates for it is most likely to be advanced when diagnosed due to its poor
indications and symptoms. Ovarian serous carcinomas are mainly divided into
different stages according to the invasiveness and metastatic ability of the tumor.
Many mutations are acquired which lead to the development of this malignancy.
This occur in entities that greatly affect the cell cycle, cell signaling pathways and
cell motility, which all involve the action of Rho GTPases. The protein of interest in
the present study was DLC2, also known as StarD13 or START-GAP2, a GTPaseactivating
protein (GAP) for Rhoa and Cdc42. Literature data indicate that this
protein is considered a tumor-suppressor in hepatocellular carcinoma. Previous
research in our laboratory confirmed StarD13 as a tumor suppressor in astrocytoma,
in breast cancer, and in colon cancer. In this study, we aim to investigate the role of
StarD13 in cell migration, invasion, and proliferation. The results show that StarD13
is a tumor suppressor in ovarian serous carcinoma, it inhibits the function of cdc42
leading to the decrease in invadopodia assembly hence hindering invasion. StarD13 is needed for cell motility via its indirect effect on RhoA activation cycle. Moreover,
StarD13 knockdown increased cell adhesiveness via the crosstalk between Cdc42
and Rac1 pathway. Therefore the cells were not being able to detach and move.
Establishing the conclusion that StarD13 is in fact a tumor suppressor but it is
needed for cell motility in ovarian cancer.
