Cancer cells that fail to be eradicated by cytotoxic therapies aimed at causing cell death can instead undergo therapy-induced senescence (TIS). Akin to cellular senescence in benign fibroblasts and epithelial cells, TIS in cancer is characterized by cell cycle arrest and an associated inflammatory secretome. While the nature of TIS is only beginning to be understood, increasing evidence suggests that is a transitory state of dormancy and cells that "escape" TIS can give rise to treatment resistance and disease recurrence.
Understanding the critical mechanisms dictating the fate of therapy-induced senescent cells is of paramount importance given the emergence of senolytic and senostatic strategies targeting TIS to treat cancer. In light of these strategies, the TIS state first needs to be comprehensively defined in different cancer cell types and their response to different therapies. Furthermore, it is imperative to explore the impact of the TIS secretome, as this can also influence the durability of cell cycle arrest., A holistic investigation of these factors will enable the full realization of the potential of exploiting TIS to minimize the likelihood of cancer relapse.
We welcome submissions that address key issues in understanding cellular components of TIS (cell cycle plasticity, epigenetic reprogramming, metabolic rewiring, heterogeneity) and interactions of senescent cancer cells with their microenvironment (stroma, microbiota, hypoxia). We also encourage contributions highlighting innovative approaches for identifying senescent cancer cells and developing functional assays for senescence escape.
Keywords:
cancer, senescence, cell cycle, dormancy, secretome, senolytic, senostatic
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
Cancer cells that fail to be eradicated by cytotoxic therapies aimed at causing cell death can instead undergo therapy-induced senescence (TIS). Akin to cellular senescence in benign fibroblasts and epithelial cells, TIS in cancer is characterized by cell cycle arrest and an associated inflammatory secretome. While the nature of TIS is only beginning to be understood, increasing evidence suggests that is a transitory state of dormancy and cells that "escape" TIS can give rise to treatment resistance and disease recurrence.
Understanding the critical mechanisms dictating the fate of therapy-induced senescent cells is of paramount importance given the emergence of senolytic and senostatic strategies targeting TIS to treat cancer. In light of these strategies, the TIS state first needs to be comprehensively defined in different cancer cell types and their response to different therapies. Furthermore, it is imperative to explore the impact of the TIS secretome, as this can also influence the durability of cell cycle arrest., A holistic investigation of these factors will enable the full realization of the potential of exploiting TIS to minimize the likelihood of cancer relapse.
We welcome submissions that address key issues in understanding cellular components of TIS (cell cycle plasticity, epigenetic reprogramming, metabolic rewiring, heterogeneity) and interactions of senescent cancer cells with their microenvironment (stroma, microbiota, hypoxia). We also encourage contributions highlighting innovative approaches for identifying senescent cancer cells and developing functional assays for senescence escape.
Keywords:
cancer, senescence, cell cycle, dormancy, secretome, senolytic, senostatic
Important Note:
All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.