Abstract
High grade serous ovarian cancer is characterized by relatively few mutations occurring at low frequency, except in TP53. However other genetic aberrations such as copy number variation alter numerous oncogenes and tumor suppressor genes. Oncogenes are positive regulators of tumorigenesis and play a critical role in cancer cell growth, proliferation, and survival. Accumulating evidence suggests that they are crucial for the development and the progression of high grade serous ovarian carcinoma (HGSOC). Though many oncogenes have been identified, no successful inhibitors targeting these molecules and their associated pathways are available. This review discusses oncogenes that have been identified recently in HGSOC using different screening strategies. All the genes discussed in this review have been functionally characterized both in vitro and in vivo and some of them are able to transform immortalized ovarian surface epithelial and fallopian tube cells upon overexpression. However, it is necessary to delineate the molecular pathways affected by these oncogenes for the development of therapeutic strategies.
Highlights
Ovarian cancer represents the most common cause of death globally due to gynecological cancer
We focus on oncogenes that were identified using strategies such as high throughput and genomic screening which were validated both in vitro and in vivo
High throughput short hairpin RiboNucleic Acid human ovarian surface epithelial cells (HOSE) (shRNA) screen performed by Project Achilles identified PAX8 as one of the potential oncogenes from 11,194 genes, which is necessary for the proliferation and survival of ovarian cancer cell lines (n = 25)
Summary
Ovarian cancer represents the most common cause of death globally due to gynecological cancer. High throughput shRNA screen performed by Project Achilles identified PAX8 as one of the potential oncogenes from 11,194 genes, which is necessary for the proliferation and survival of ovarian cancer cell lines (n = 25). Knockdown of PAX8 in ovarian cancer cells with amplification or overexpression of this gene resulted in reduced viability, but not in cell lines without any alterations of this gene [24].
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