About this Research Topic
Cell suicide pathways, termed regulated cell death (RCD), play critical roles in organismal development, homeostasis, and pathogenesis. Increasing evidence suggests that RCD subroutines are key features of tumorigenesis, which may ultimately lead to the establishment of different potential therapeutic strategies. Ferroptosis is driven by iron-dependent phospholipid peroxidation and regulated by multiple cellular metabolic pathways, including redox homeostasis, iron handling, mitochondrial activity, metabolism of amino acids, lipids, and sugars, as well as various disease-related signaling pathways. Treatment-resistant cancer cells, especially those in a stromal state and prone to metastasis, are highly susceptible to ferroptosis. Curroptosis is a copper- and mitochondria-dependent independent cell death mechanism. Pan-apoptosis is controlled by a recently discovered cytoplasmic polyprotein complex called the PANoptosome. PANoptosomes can simultaneously participate in the three key modes of programmed cell death—pyroptosis, apoptosis, and necroptosis. PANoptosome components have been implicated in a variety of human diseases, including autoinflammatory diseases, neurodegenerative diseases, cancer, microbial infections, and metabolic diseases. This research topic is to provide a forum to advance research on the effects of tumor disease development and progression and to explore the remodeling of the tumor immune microenvironment by emerging regulatory cell death modes, including ferroptosis, curroptosis, and pan-apoptosis, to have a beneficial impact on the neoplastic disease by facilitating crosstalk between tumor progression and treatment.
Topics include, but are not limited to:
1) Biomarkers and mechanisms of curroptosis, ferroptosis, or pan-apoptosis in inflammatory diseases
2) Complex effects of emerging forms of tumor cell death on the immune microenvironment, as well as the regulated death of other cells in the immune microenvironment that affect tumor biology
3) Combination study of the crosstalk effects of curroptosis, ferroptosis, and pan-apoptosis in tumor progression and treatment
4) The potential novel drugs and nanoparticles to induce or inhibit new RCD pathways and their therapeutic effects on cancer
5) Effects of modulating RCD processes on cancer drug resistance
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Topics include, but are not limited to:
1) Biomarkers and mechanisms of curroptosis, ferroptosis, or pan-apoptosis in inflammatory diseases
2) Complex effects of emerging forms of tumor cell death on the immune microenvironment, as well as the regulated death of other cells in the immune microenvironment that affect tumor biology
3) Combination study of the crosstalk effects of curroptosis, ferroptosis, and pan-apoptosis in tumor progression and treatment
4) The potential novel drugs and nanoparticles to induce or inhibit new RCD pathways and their therapeutic effects on cancer
5) Effects of modulating RCD processes on cancer drug resistance
Please note: manuscripts consisting solely of bioinformatics or computational analysis of public genomic or transcriptomic databases which are not accompanied by validation (independent cohort or biological validation in vitro or in vivo) are out of scope for this section and will not be accepted as part of this Research Topic.
Keywords: Emerging cell death, immune microenvironment remodeling, RCD, regulated cell death, Curroptosis, ferroptosis, pan-apoptosis
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.
