bioRxiv · 10.1101/2024.08.22.609150
CDK4/6 inhibitors promote senescence-associated lysosomal alterations and enhance sensitivity to lysosomotropic agents in breast cancer
Abstract
Breast cancer is a leading cause of mortality worldwide. Pharmacological inhibitors of Cyclin- Dependent Kinases (CDK) 4 and 6 (CDK4/6i) inhibit breast cancer growth by inducing a senescent-like state. However, the long-term treatment efficacy remains hindered by the development of drug resistance. Clearance of senescent-like cancer cells may extend the durability of treatment. In this study, we showed that CDK4/6i-treated breast cancer cells exhibit various senescence-associated phenotypes, but remain insensitive to common senolytic compounds. By searching for novel vulnerabilities, we identified a significantly increased lysosomal mass and altered lysosomal structure across various breast cancer cell types upon exposure to CDK4/6i in preclinical systems and clinical specimens. We demonstrated that these lysosomal alterations render breast cancer cells sensitive to lysosomotropic agents, such as L- leucyl-L-leucine methyl ester (LLOMe) and salinomycin. Importantly, sequential treatment with CDK4/6i/lysosomotropic agents effectively reduced the growth of both Hormone Receptor- positive (HR+) and triple-negative breast cancer (TNBC) cells in vivo. This sequential therapeutic strategy offers a promising approach to eliminate CDK4/6i-induced senescent(-like) cells, potentially reducing tumor recurrence and enhancing the overall efficacy of breast cancer therapy.
Source connections
Explore related subjects
Keep this discovery
Explore connections, maps & timelines
Nehme, J., Massen, S., Bravaccini, S., Zanoni, M., Gianni, C., De Giorgi, U., Soto-Gamez, A., Altulea, A., Gheorghe, T., Wang, B., Demaria, M.. 2024-08-23. CDK4/6 inhibitors promote senescence-associated lysosomal alterations and enhance sensitivity to lysosomotropic agents in breast cancer. https://doi.org/10.1101/2024.08.22.609150
Cite the original work for its findings. Save a collection to share your selection of sources.