Targeting CDK9: A novel biomarker in the treatment of endometrial cancer
- Shasha He
- Xiaoling Fang
- Xiaomeng Xia
- Tao Hou
- Tingting Zhang
Affiliations: Department of Oncology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410000, P.R. China, Department of Obstetrics and Gynecology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410000, P.R. China
- Published online on: September 1, 2020 https://doi.org/10.3892/or.2020.7746
Copyright: © He
et al. This is an open access article distributed under the
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Endometrial cancer is one of the three major malignant tumors of the female reproductive system. Although cyclin‑dependent kinase 9 (CDK9) has a definitive pathogenic role in various types of cancer, little is known concerning its function in endometrial cancer. Our study was conducted to evaluate the expression and therapeutic potential of CDK9 in endometrial cancer. CDK9 expression was determined by immunohistochemistry in endometrial cancer tissues constructed with paired primary, metastatic, and recurrent tumor tissues from 32 endometrial cancer patients. Small interfering RNA (siRNA) and inhibitors of CDK9 were used to evaluate the effect of CDK9 inhibition on the anti‑apoptotic activity and proliferation in endometrial cancer cells. Colony formation assay and wound‑healing assays were adopted to assess clonal formation and migratory capacity. The results of the immunohistochemistry demonstrated that CDK9 was highly expressed in the human endometrial cancer cell lines; moreover, it was elevated in metastatic and recurrent endometrial tumor tissue compared when compared with that in patient‑matched primary endometrial tumor tissue. Knockdown of CDK9 with siRNA and inhibition of CDK9 activity with the inhibitor suppressed cell proliferation and promoted apoptosis in endometrial cancer. In conclusion, our results provide evidence that CDK9 may be a potential prognostic biomarker and a promising therapeutic target for the treatment of endometrial cancer in the future.