Ovarian cancer and aurora kinases

Key controllers of mitotic spindle formation are aurora kinases (AURK). In ovarian cancer, AURK is typically overexpressed, and this overexpression has frequently been linked to prognosis in these tumors. Interesting interactions between AURK and other cell cycle regulators and DNA repair processes have been discovered.

The Aurora family has emerged as a possible target for anticancer treatment as a result of these capabilities. Two clinical studies using various AURK inhibitors in recent years have demonstrated efficacy in treating epithelial and clear-cell ovarian cancer.

Despite the absence of predictors of AURK inhibitory action, subsequent studies have shown several potential possibilities. The activities of the AURK family, its function as a prognostic factor in epithelial ovarian cancer, and potential therapeutic consequences will be the main topics of this review.

The primary function of the family of serin-threonin kinases known as aurora kinases (AURK) is the control of mitotic spindle formation. Aurora kinase A (AURKA, STK15), Aurora kinase B (AURKB, STK12), and Aurora kinase C are all members of the AURK family (AURKC, STK13).

Recent research has shown that the AURK family is involved not only in the mitotic process but also in the control of the cell cycle, including chromosomal segregation failure, which results in genetic instability, polyploidy, and a markedly higher incidence of tumors.

The homologous structure of AURK, which consists of a protein kinase domain, an N-terminal domain, and a well preserved C-terminal region, is highly conserved. Overexpression or amplification of members of the AURK family is a frequent change in cancer. AURKA overexpression is linked to ki67, proliferation, and a basal-like phenotype in breast cancer, whereas AURKB is linked to ki67, histological grade, and other factors.

Other tumor forms in which AURKA and AURKB overexpression or amplification have been reported and linked to unfavorable clinical characteristics include gliomas, prostate cancer, cervical cancer, and lung cancer. It was discovered that AURKC overexpression and tumor grade were related with colorectal cancer.

AURK is typically overexpressed in epithelial ovarian cancer (EOC), and multiple published series have demonstrated that its expression has an effect on prognosis. The AURK family is involved in DNA repair, cell cycle control, and mitosis. It has been proposed that the AURKA-BRCA2 balance controls tumorigenesis.

Preclinical research also hints that the AURK family may be involved in the processes of chemoresistance. Additionally, the AURK family has developed as a possible target for cancer precision treatment. AURK inhibitors have been created and evaluated in several cancer types during the past ten years. AURK inhibitors have also been explored in EOC, with varying outcomes.

EOC and clear-cell ovarian cancer have both demonstrated efficacy in two recent therapeutic studies using various AURK inhibitors (OC). Mutations in the ARID1a gene have been discovered as a possible biomarker that might predict the inhibition of AURK in this subtype.


The AURK family is crucial to the development of tumors in OC. AURKA overexpression or amplification is a frequent change in EOC that has an impact on the prognosis. AURK, however, has emerged as a possible target in recent years because to some encouraging outcomes from AURK inhibitors such alisertib and ENMD-2076. The toxicity of several of these drugs, which may be important when paired with chemotherapy, is the main issue for continued research.

However, there is a critical need to keep investigating the AURK pathway’s therapeutic potential in this situation.

Note: In accordance with that hypothesis, you may browse the Chemdiv Compound Collection’s collection of potentially selective Aurora A kinase inhibitors here. In the aurora libraries, there are about 10,000 different compounds.


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