The Role of Cyclin E. in Ovarian Cancer

Role of Cyclin E in Ovarian Cancer Cell cycle control involves a range of proteins. Defects in these proteins can result in cell malignancies. Overexpression of Cyclin E characterizes a subset of epithelia ovarian tumors, which are a major cause of death among women. Studies have indicated that deregulation of the levels of Cyclin E results in chromosomal instability, which a critical characteristic of epithelial ovarian malignancies (Vaughan et al., 2011). This indicates that deregulation of Cyclin E is a critical occurrence in ovarian carcinogenesis.

Therefore, improper regulation of Cyclin E can cause increased multiplication and genomic imbalance, which can stimulate cancer. In particular, deregulation of Cyclin E through increased activity can trigger ovarian, colon, and prostate cancers (Vaughan et al., 2011).

Cyclin E plays an active role in several stages of tumorigenesis from initial transformation to metastasis. Cyclin E gene amplification in ovarian cancer has been described in 12-21 percent of ovarian tumors. For this reason, its connection to patient outcomes in ovarian cancers has been assessed through an assortment of studies because of its overexpression properties.

Through the activation of CDK2, Cyclin E leads to several aspects of tumorigenesis that include higher multiplication, anchorage independent growth, amplification of centrosome, genomic imbalance, and metastasis (Vaughan et al., 2011). It is overexpressed in high-grade serous epithelial ovarian tumors in case of severe epithelia ovarian cancer. This gene is cleaved post-transnationally into oncogenic tumor-specific low molecular weight isoforms known as LMW-E (Vaughan et al., 2011). These isoforms of Cyclin E are tumor-specific and are characterized by the capacity to hyper-activate CDK2.

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Consequently, the overexpression of PKCiota in severe epithelial tumors relates to the presence of LMW-E. For this reason, PKCiota is a feasible target for therapy in serous ovarian cancer, especially through deregulation of other oncogenes such as Cyclin E. therefore, Cyclin E is a downstream of PKCiota and thus, the effect of PKCiota on the overexpression of Cyclin E leads to protein stability.