UVRAG: A new player in autophagy and tumor cell growth
Open accessAbstract
Autophagy has a well-documented role in the maintenance of homeostasis and the response to stressful environments and it is often deregulated in various human diseases including cancer. The regulation of the Beclin 1-PI3KC3 complex lipid kinase activity is a critical element in the autophagy signaling pathway. Previous studies1 have demonstrated that Beclin 1-PI3KC3-mediated autophagy is negatively regulated by a proto-oncogene Bcl-2. We have recently identified a novel coiled-coil UVRAG tumor suppressor candidate, which positively engages in Beclin 1-dependent autophagy. UVRAG interacts with Beclin 1, leading to activation of autophagy and thereof inhibition of tumorigenesis. This finding adds a new player to the emerging picture of the autophagy network, underscoring the importance of the coordinated activity between Bcl-2 and UVRAG in the regulation of Beclin 1-PI3KC3- mediated autophagy and tumor cell control.Addendum to:Autophagic and Tumor Suppressor Activity of a Novel Beclin 1-Binding Protein UVRAGChengyu Liang, Pinghui Feng, Bonsu Ku, Iris Dotan, Dan Canaani, Byung-Ha Oh and Jae U. JungNature Cell Biol 2006; 8:688-99
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AMPK regulates macroautophagy.
“or through the regulation of macroautophagy (Buzzai et al. 2007; J. Liang et al. 2007;Lippai et al. 2008).”
From Tumor suppressors and cell metabolism: a recipe for cancer growth (2009) · cites this paper as J. Liang et al. 2007
UVRAG and Bif display tumor suppressor properties.
“Other modifiers of Beclin-1 activity such as UVRAG and Bif display tumor suppressor properties (C.Liang et al. 2007;Takahashi et al. 2007)”
From Tumor suppressors and cell metabolism: a recipe for cancer growth (2009) · cites this paper as C.Liang et al. 2007
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“UVRAG promotes autophagy by regulating Beclin 1-PI3KC3 complex as a positive mediator [5] and suppresses Bax-induced apoptosis by influencing the location of Bax [6].”
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“For example, ultraviolet-radiation-resistance-associated gene, which positively regulates Beclin-1 to induce autophagy, is monoallelically mutated at high frequency in human colon cancers (120,123).”
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Autophagy-Independent Tumor Suppression
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Self-citationMolecular Mechanism of AGC Kinases in Human Malignant
Shu, S. (2010) · Digital Commons - University of South Florida (University of South Florida) · Cited by 1 · see citing works
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Investigating the function of NR4A3 in melanocyte DNA repair and cyto-protection
Pavarino, A. C. D. A. (2024) · Queensland University of Technology · doi:10.5204/thesis.eprints.248364
Zhou, S., Liu, J., Hu, M., Tian, S., Zhou, J., Li, W., Chen, H., Yin, M., Wang, S., Luo, L., et al. (2026) · Circulation · doi:10.1161/circulationaha.125.077971
- Authors
- Liang, C., Feng, P., Ku, B., Oh, B.-H., & Jung, J. U.
- Affiliations
- Harvard University (US)
- Pohang University of Science and Technology (KR)
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2007-01-08
- Volume
- 3
- Issue
- 1
- Pages
- 69-71
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- OpenAlex
- W2026526405
- Cited by
- 76
- References
- 0
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 2 · 2023: 1 · 2022: 1 · 2021: 3 · 2020: 6 · 2019: 3 · 2018: 3 · 2017: 4 · 2016: 4 · 2015: 3 · 2014: 9 · 2013: 6 · 2012: 4
- FWCI
- 4.59
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed (publishedVersion)
- Open Access System for Information Sharing (Pohang University of Science and Technology) (submittedVersion)
- Topics
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ubiquitin and proteasome pathways
- Keywords
- UVRAG, Beclin-1, Bcl-2, tumor suppressor, coiled-coil proteins, carcinogenesis, protein-protein interaction
- MeSH terms
- Proto-Oncogene Mas, Animals, Autophagy, Humans, Neoplasms, Tumor Suppressor Proteins, Cell Growth Processes
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