Actin Cytoskeleton Dynamics and Type I IFN-Mediated Immune Response: A Dangerous Liaison in Cancer?

Simple Summary Actin cytoskeleton is a dynamic subcellular component critical for maintaining cell shape and for elaborating response to any stimulus converging on the cell. Cytoskeleton constantly interfaces with diverse cellular components and affects a wide range of processes important in homeostasis and disease. What has been clearly demonstrated to date is that pathogens modify and use host cytoskeleton to their advantage. What is now emerging is that in sterile conditions, when a chronic inflammation occurs as in cancer, the subversion of tissue homeostasis induces an alarm status which mimics infection. This activates cellular players similar to those that solve an infection, but their persistence may pave the way for tumor progression. Understanding molecular mechanisms engaged by cytoskeleton to induce this viral mimicry could improve our knowledge of processes governing tumor progression and resistance to therapy. Chronic viral infection and cancer are closely inter-related and are both characterized by profound alteration of tissue homeostasis. The actin cytoskeleton dynamics highly participate in tissue homeostasis and act as a sensor leading to an immune-mediated anti-cancer and anti-viral response. Herein we highlight the crucial role of actin cytoskeleton dynamics in participating in a viral mimicry activation with profound effect in anti-tumor immune response. This still poorly explored field understands the cytoskeleton dynamics as a platform of complex signaling pathways which may regulate Type I IFN response in cancer. This emerging network needs to be elucidated to identify more effective anti-cancer strategies and to further advance the immuno-oncology field which has revolutionized the cancer treatment. For a progress to occur in this exciting arena we have to shed light on actin cytoskeleton related pathways and immune response. Herein we summarize the major findings, considering the double sword of the immune response and in particular the role of Type I IFN pathways in resistance to anti-cancer treatment.

Automated summary

The actin cytoskeleton plays a crucial role in maintaining cell shape and responding to stimuli, but can also be exploited by pathogens, leading to cellular dysfunction. Chronic inflammation and cancer can induce a viral mimicry alarm status through modulation of the cytoskeleton, promoting tumor progression. Understanding the molecular mechanisms of cytoskeleton-mediated viral mimicry is critical for developing effective anti-cancer strategies in the rapidly advancing field of immuno-oncology.