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Updated: May 21, 2026
Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Cell death signaling and anticancer therapy
Lorenzo Galluzzi1, Ilio Vitale, Erika Vacchelli
1INSERM U848 Villejuif, France.
Abstract:
For a long time, it was commonly believed that efficient anticancer regimens would either trigger the apoptotic demise of tumor cells or induce a permanent arrest in the G(1) phase of the cell cycle, i.e., senescence. The recent discovery that necrosis can occur in a regulated fashion and the increasingly more precise characterization of the underlying molecular mechanisms have raised great interest, as non-apoptotic pathways might be instrumental to circumvent the resistance of cancer cells to conventional, pro-apoptotic therapeutic regimens. Moreover, it has been shown that some anticancer regimens engage lethal signaling cascades that can ignite multiple oncosuppressive mechanisms, including apoptosis, necrosis, and senescence. Among these signaling pathways is mitotic catastrophe, whose role as a bona fide cell death mechanism has recently been reconsidered. Thus, anticancer regimens get ever more sophisticated, and often distinct strategies are combined to maximize efficacy and minimize side effects. In this review, we will discuss the importance of apoptosis, necrosis, and mitotic catastrophe in the response of tumor cells to the most common clinically employed and experimental anticancer agents.
Insights
Anticancer treatments are evolving beyond apoptosis and senescence. New research highlights regulated necrosis and mitotic catastrophe as key cell death pathways to overcome cancer resistance and improve therapeutic efficacy.
Area of Science:
- Oncology
- Cell Biology
- Molecular Medicine
Background:
- Traditionally, anticancer strategies focused on apoptosis and G1 cell cycle arrest (senescence).
- Emerging research reveals regulated necrosis and mitotic catastrophe as significant cell death mechanisms.
- These alternative pathways offer potential to bypass cancer cell resistance to conventional therapies.
Purpose of the Study:
- To review the significance of apoptosis, necrosis, and mitotic catastrophe in tumor cell responses.
- To discuss the role of these cell death pathways in relation to anticancer agents.
- To highlight the evolving landscape of cancer therapeutics.
Main Methods:
- Literature review of established and experimental anticancer agents.
- Analysis of molecular mechanisms underlying apoptosis, necrosis, and mitotic catastrophe.
- Discussion of clinical implications and therapeutic strategies.
Main Results:
- Anticancer agents can induce multiple cell death pathways simultaneously.
- Regulated necrosis and mitotic catastrophe are increasingly recognized as critical for overcoming treatment resistance.
- Sophisticated therapeutic regimens combine distinct strategies to enhance efficacy and reduce side effects.
Conclusions:
- Apoptosis, necrosis, and mitotic catastrophe are crucial determinants of tumor cell response to anticancer treatments.
- Understanding these diverse cell death mechanisms is vital for developing novel and effective cancer therapies.
- The integration of multiple cell death-inducing strategies represents the future of advanced cancer treatment.
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