Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression. (4th April 2013)
- Record Type:
- Journal Article
- Title:
- Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression. (4th April 2013)
- Main Title:
- Endocytic Adaptor Protein Epsin Is Elevated in Prostate Cancer and Required for Cancer Progression
- Authors:
- Tessneer, Kandice L.
Pasula, Satish
Cai, Xiaofeng
Dong, Yunzhou
Liu, Xiaolei
Yu, Lili
Hahn, Scott
McManus, John
Chen, Yiyuan
Chang, Baojun
Chen, Hong - Other Names:
- Akiyama Y. Academic Editor.
Bentel J. Academic Editor.
Guo Z. S. Academic Editor.
Yu Y. Academic Editor. - Abstract:
- Abstract : Epsins have an important role in mediating clathrin-mediated endocytosis of ubiquitinated cell surface receptors. The potential role for epsins in tumorigenesis and cancer metastasis by regulating intracellular signaling pathways has largely not been explored. Epsins are reportedly upregulated in several types of cancer including human skin, lung, and canine mammary cancers. However, whether their expression is elevated in prostate cancer is unknown. In this study, we investigated the potential role of epsins in prostate tumorigenesis using the wild type or epsin-deficient human prostate cancer cells, LNCaP, in a human xenograft model, and the spontaneous TRAMP mouse model in wild type or epsin-deficient background. Here, we reported that the expression of epsins 1 and 2 is upregulated in both human and mouse prostate cancer cells and cancerous tissues. Consistent with upregulation of epsins in prostate tumors, we discovered that depletion of epsins impaired tumor growth in both the human LNCaP xenograft and the TRAMP mouse prostate. Furthermore, epsin depletion significantly prolonged survival in the TRAMP mouse model. In summary, our findings suggest that epsins may act as oncogenic proteins to promote prostate tumorigenesis and that depletion or inhibition of epsins may provide a novel therapeutic target for future prostate cancer therapies.
- Is Part Of:
- ISRN oncology. Volume 2013(2013)
- Journal:
- ISRN oncology
- Issue:
- Volume 2013(2013)
- Issue Display:
- Volume 2013, Issue 2013 (2013)
- Year:
- 2013
- Volume:
- 2013
- Issue:
- 2013
- Issue Sort Value:
- 2013-2013-2013-0000
- Page Start:
- Page End:
- Publication Date:
- 2013-04-04
- Subjects:
- Oncology -- Periodicals
Neoplasms
Oncology
Periodicals
616.994 - Journal URLs:
- https://www.hindawi.com/journals/isrn/contents/isrn.oncology/ ↗
- DOI:
- 10.1155/2013/420597 ↗
- Languages:
- English
- ISSNs:
- 2090-5661
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library HMNTS - ELD Digital store
- Ingest File:
- 10614.xml