Research Papers:

RNPC1 enhances progesterone receptor functions by regulating its mRNA stability in breast cancer

Peipei Lou, Chunlian Li, Liang Shi, Tian-Song Xia, Wenbin Zhou, Jing Wu, Xujie Zhou, Xiaoxia Li, Ying Wang, Ji-Fu Wei _ and Qiang Ding

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Oncotarget. 2017; 8:16387-16400. https://doi.org/10.18632/oncotarget.12016

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Peipei Lou1,*, Chunlian Li1,*, Liang Shi1,*, Tian-Song Xia1, Wenbin Zhou1, Jing Wu1, Xujie Zhou1, Xiaoxia Li1, Ying Wang1, Ji-Fu Wei2, Qiang Ding1

1Jiangsu Breast Disease Center, The First Affiliated Hospital with Nanjing Medical University, Nanjing City, Jiangsu Province, 210000, China

2Research Division of Clinical Pharmacology, The First Affiliated Hospital with Nanjing Medical University, Nanjing City, Jiangsu Province, 210000, China

*These authors have contributed equally to this work

Correspondence to:

Ji-Fu Wei, email: [email protected]

Qiang Ding, email: [email protected]

Keywords: progesterone receptor, RNPC1, mRNA stability, breast cancer, proliferation

Received: January 04, 2016     Accepted: July 26, 2016     Published: September 14, 2016


Progesterone receptor (PR) could activate transcriptional process involved in normal mammary gland proliferation and breast cancer development. Moreover, PR expression is an important marker of luminal breast cancer, which is associated with good prognosis and indicates better responding to endocrine therapies. The regulation of PR expression was studied mainly on its post-translational levels. In this study, we found PR was positively regulated by RNA-binding region-containing protein 1 (RNPC1), a RNA-binding protein, in PR positive breast cancer. Overexpression of RNPC1 increased, whereas knockdown of RNPC1 decreased, the level of PR protein and transcripts. Additionally, we demonstrated that RNPC1 could bind to PR mRNA via AU-rich elements (AREs) within PR 3′-untranslated region (3′-UTR) and then enhance PR mRNA stability. Moreover, we proved that progesterone-dependent PR functions which could induce breast cancer proliferation were enhanced by RNPC1, both in vitro and in vivo. Conclusively, we revealed a novel mechanism by which PR could be regulated by RNPC1 via stabilizing its mRNA.

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