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Updated: Aug 19, 2026
SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
Published on: June 28, 2019
Targeting senescence pathways to reverse drug resistance in cancer
1Children's Memorial Research Center, M/C 224, Children's Memorial Hospital, and Department of Pediatrics, Feinberg School of Medicine, Northwestern University, 2300 Children's Plaza, Chicago, IL 60614, USA. arebbaa@childrensmemorial.org
Abstract:
Irreversible proliferation arrest (also called senescence) has emerged recently as a drug-responsive program able to influence the outcome of cancer chemotherapy. Since the drug amounts required for induction of proliferation arrest are much lower than those necessitated for induction of cell death, forcing cancer cells to undergo senescence may represent a less aggressive approach to control tumor progression. However, to achieve a long-standing control of proliferation, the ability of cancer cells to escape senescence and become drug resistant must be inhibited. Therefore, a clear understanding of the mechanisms that govern drug-induced senescence is critical and can lead to discovery of novel approaches to suppress drug resistance. The present review discusses the relevance of senescence in response to chemotherapy and the onset of drug resistance development. Particular emphasis is directed toward the utilization of findings from the field of research on aging, that can be applied to induction of senescence in cancer cells and reversal of their drug resistance phenotype. Proof of principle for this relationship is represented by the identification of inhibitors of aging associated proteases such as the proteasome and cathepsin L as novel and potent cancer drug resistance reversing agents.
Insights
Inducing cancer cell senescence, a reversible proliferation arrest, offers a less aggressive chemotherapy approach. Inhibiting senescence escape and drug resistance is key, with aging research providing novel strategies.
Area of Science:
- Oncology
- Cellular Biology
- Aging Research
Background:
- Senescence, or irreversible proliferation arrest, is a drug-responsive cancer chemotherapy mechanism.
- Inducing senescence requires lower drug doses than cell death induction, offering a less aggressive tumor control strategy.
- Cancer cells can escape senescence and develop drug resistance, necessitating inhibition strategies.
Purpose of the Study:
- To review the role of senescence in chemotherapy response and drug resistance.
- To explore how aging research can inform cancer senescence induction and drug resistance reversal.
- To identify novel approaches for suppressing drug resistance in cancer cells.
Main Methods:
- Review of existing literature on drug-induced senescence and cancer chemotherapy.
- Analysis of findings from aging research applicable to cancer cell senescence.
- Identification of molecular targets for reversing drug resistance.
Main Results:
- Senescence induction is a viable, less aggressive approach to cancer chemotherapy.
- Understanding senescence mechanisms is critical for overcoming drug resistance.
- Inhibitors of aging-associated proteases, like proteasome and cathepsin L, reverse cancer drug resistance.
Conclusions:
- Targeting senescence offers a promising avenue for cancer treatment.
- Leveraging aging research can lead to novel strategies against cancer drug resistance.
- Proteasome and cathepsin L inhibitors show potential as cancer drug resistance reversing agents.
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