Research Paper Volume 13, Issue 8 pp 11822—11832
ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203
- 1 Maternity Service Center of Pengzhou Maternal & Children Health Care Hospital, Chengdu, Sichuan Province 611930, People’s Republic of China
- 2 Department of Hepatobiliary and Pancreatic Surgery, Huai’an First People’s Hospital, Nanjing Medical University, Huai'an 223300, Jiangsu Province, People’s Republic of China
- 3 Hainan Maternal and Children’s Medical Center, Haikou 570206, Hainan Province, People’s Republic of China
- 4 Department of Pathology, The Affiliated Hospital of Hainan Medical University, Haikou 571101, Hainan Province, People’s Republic of China
Received: November 16, 2020 Accepted: March 14, 2021 Published: April 20, 2021https://doi.org/10.18632/aging.202880
How to Cite
Copyright: © 2021 Shaosheng et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Overcoming senescence is a feature of ovarian cancer cells; however, the mechanisms underlying senescence regulation in ovarian cancer cells remain largely unknown. In this study, we found that ITPKA was downregulated in ovarian cancer samples, and the lower expression correlated with poor survival. Overexpression of ITPKA inhibited the anchorage-independent growth of ovarian cancer cells and induced senescence. However, knockdown of ITPKA promoted the anchorage-independent growth of ovarian cancer cells and inhibited senescence. Mechanistically, ITPKA was found to interact with MDM2, which stabilized P53, an essential regulator of senescence. Moreover, ITPKA was negatively regulated by miR-203, a microRNA that has been previously reported to be upregulated in ovarian cancer. Taken together, the results of this study demonstrated the tumor suppressive roles of ITPKA in ovarian cancer and provided a good explanation for the oncogenic roles of miR-203.