Journal
TRENDS IN CELL BIOLOGY
Volume 26, Issue 1, Pages 17-28Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2015.10.011
Keywords
-
Categories
Funding
- Jackson Laboratory Cancer Center Support Grant [3P30CA034196]
- National Institutes of Health [1DP2OD007070, R21CA184704]
- Ellison Medical Foundation [AS-NS-0599-09]
- NATIONAL CANCER INSTITUTE [P30CA034196, R21CA184704] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [DP2OD007070] Funding Source: NIH RePORTER
Ask authors/readers for more resources
Proteomic instability is causally related to human diseases. In guarding proteome stability, the heat shock factor 1 (HSF1)-mediated proteotoxic stress response plays a pivotal role. Contrasting with its beneficial role of enhancing cell survival, recent findings have revealed a compelling pro-oncogenic role for HSF1. However, the mechanisms underlying the persistent activation and function of HSF1 within malignancy remain poorly understood. Emerging evidence reveals that oncogenic signaling mobilizes HSF1 and that cancer cells rely on HSF1 to avert proteomic instability and repress tumor-suppressive amyloidogenesis. In aggregate, these new developments suggest that cancer cells endure chronic proteotoxic stress and that proteomic instability is intrinsically associated with the malignant state, a characteristic that could be exploited to combat cancer.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available