Journal article
IRE1α-XBP1s pathway promotes prostate cancer by activating c-MYC signaling
- Abstract:
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Activation of endoplasmic reticulum (ER) stress/the unfolded protein response (UPR) has been linked to cancer, but the molecular mechanisms are poorly understood and there is a paucity of reagents to translate this for cancer therapy. Here, we report that an IRE1α RNase-specific inhibitor, MKC8866, strongly inhibits prostate cancer (PCa) tumor growth as monotherapy in multiple preclinical models in mice and shows synergistic antitumor effects with current PCa drugs. Interestingly, global tran...
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- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 2.5MB, Terms of use)
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- Publisher copy:
- 10.1038/s41467-018-08152-3
Authors
Bibliographic Details
- Publisher:
- Springer Nature
- Journal:
- Nature Communications More from this journal
- Volume:
- 10
- Article number:
- 323
- Publication date:
- 2019-01-24
- Acceptance date:
- 2018-12-07
- DOI:
- EISSN:
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2041-1723
- Pmid:
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30679434
Item Description
- Language:
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English
- Pubs id:
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pubs:966369
- UUID:
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uuid:999dfe25-8723-4cdb-9ee3-b93a35858521
- Local pid:
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pubs:966369
- Source identifiers:
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966369
- Deposit date:
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2019-01-28
Terms of use
- Copyright holder:
- Sheng et al
- Copyright date:
- 2019
- Notes:
- © The Author(s) 2019. This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
- Licence:
- CC Attribution (CC BY)
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