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ITPKA 诱导细胞衰老，抑制卵巢癌发生，其表达可被 miR-203 下调。

ITPKA induces cell senescence, inhibits ovarian cancer tumorigenesis and can be downregulated by miR-203.

机构信息

Maternity Service Center of Pengzhou Maternal & Children Health Care Hospital, Chengdu, Sichuan Province 611930, People's Republic of China.

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.

出版信息

Aging (Albany NY). 2021 Apr 20;13(8):11822-11832. doi: 10.18632/aging.202880.

DOI:10.18632/aging.202880
PMID:33879633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8109125/
Abstract

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.

摘要

克服衰老性是卵巢癌细胞的一个特征；然而，卵巢癌细胞衰老性调控的机制在很大程度上仍然未知。在这项研究中，我们发现 ITPKA 在卵巢癌样本中表达下调，较低的表达与较差的生存相关。ITPKA 的过表达抑制了卵巢癌细胞的非锚定依赖性生长并诱导了衰老。然而，ITPKA 的敲低促进了卵巢癌细胞的非锚定依赖性生长并抑制了衰老。从机制上讲，发现 ITPKA 与 MDM2 相互作用，MDM2 稳定了 P53，P53 是衰老的一个重要调节因子。此外，ITPKA 受到 miR-203 的负调控，miR-203 是一种先前报道在卵巢癌中上调的 microRNA。总之，这项研究的结果表明 ITPKA 在卵巢癌中具有肿瘤抑制作用，并为 miR-203 的致癌作用提供了很好的解释。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/c26d31ef968e/aging-13-202880-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/431900f71e13/aging-13-202880-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/b788a90e055c/aging-13-202880-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/e449b104ab0e/aging-13-202880-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/429a666e93bf/aging-13-202880-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/c26d31ef968e/aging-13-202880-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/431900f71e13/aging-13-202880-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/b788a90e055c/aging-13-202880-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/e449b104ab0e/aging-13-202880-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/429a666e93bf/aging-13-202880-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7eec/8109125/c26d31ef968e/aging-13-202880-g005.jpg

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