Journal
ISCIENCE
Volume 23, Issue 9, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.isci.2020.101470
Keywords
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Categories
Funding
- Swedish Research Council [K2019-01598, 2015-02756]
- Swedish Cancer Society [CAN 2017/544, 18 0491, 2016/445]
- Umea University [ALF-VLL-464591, ALF-VLL-583901]
- Region Vasterbotten (RV
- ALF) [ALF-VLL-464591, ALF-VLL-583901]
- Knut and Alice Wallenberg Foundation [2012.0090]
- Prostatacancerforbundet
- Novo Nordisk Foundation XPS Extension Grant [59307]
- Kempe Foundation
- Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse
- Lion's Cancer Research Foundation
- Umea University
- European Research Council [787472]
- Swedish Cancer Society
- [RV 933125]
- [RV 738911]
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Transforming growth factor beta (TGF-beta) enhances migration and invasion of cancer cells, causing life-threatening metastasis. Smad7 expression is induced by TGF-beta to control TGF-beta signaling in a negative feedback manner. Here we report an additional function of Smad7, i.e., to enhance TGF-beta induction of c-Jun and HDAC6 via binding to their regulatory regions, promoting migration and invasion of prostate cancer cells. Lysine 102 in Smad7 is crucial for binding to specific consensus sites in c-Jun and HDAC6, even when endogenous Smad2, 3, and 4 were silenced by siRNA. A correlation between the mRNA expression of Smad7 and HDAC6, Smad7 and c-Jun, and c-Jun and HDAC6 was found in public databases from analyses of prostate cancer tissues. High expression of Smad7, HDAC6, and c-Jun correlated with poor prognosis for patients with prostate cancer. The knowledge that Smad7 can activate transcription of proinvasive genes leading to prostate cancer progression provides clinically relevant information.
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