Research Paper Volume 15, Issue 7 pp 2373—2394
Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic
- 1 Mechanisms of Cancer and Aging Laboratory, University of Leicester, Leicester LE1 7RH, United Kingdom
- 2 Department of Molecular and Cell Biology, University of Leicester, Leicester LE1 7RH, United Kingdom
- 3 Clinical Laboratory Sciences Department, College of Applied Medical Sciences, Najran University, Najran 11001, Kingdom of Saudi Arabia
- 4 The Ernest and Helen Scott Haematological Research Institute, University of Leicester, Leicester LE1 7RH, United Kingdom
- 5 FoodLab, Faculty of Health Sciences, Universitat Oberta de Catalunya, Barcelona 08018, Spain
Received: November 21, 2022 Accepted: March 17, 2023 Published: March 28, 2023
https://doi.org/10.18632/aging.204616How to Cite
Copyright: © 2023 Al-Mansour et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
The accumulation of senescent cells has an important role in the phenotypical changes observed in ageing and in many age-related pathologies. Thus, the strategies designed to prevent these effects, collectively known as senotherapies, have a strong clinical potential. Senolytics are a type of senotherapy aimed at specifically eliminating senescent cells from tissues. Several small molecule compounds with senolytic properties have already been identified, but their specificity and range of action are variable. Because of this, potential novel senolytics are being actively investigated. Given the involvement of HDACs and the PI3K pathway in senescence, we hypothesized that the dual inhibitor CUDC-907, a drug already in clinical trials for its antineoplastic effects, could have senolytic effects. Here, we show that CUDC-907 was indeed able to selectively induce apoptosis in cells driven to senesce by p53 expression, but not when senescence happened in the absence of p53. Consistent with this, CUDC-907 showed senolytic properties in different models of stress-induced senescence. Our results also indicate that the senolytic functions of CUDC-907 depend on the inhibitory effects of both HDACs and PI3K, which leads to an increase in p53 and a reduction in BH3 pro-survival proteins. Taken together, our results show that CUDC-907 has the potential to be a clinically relevant senolytic in pathological conditions in which stress-induced senescence is involved.