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Manuscript Submission Deadline 05 October 2022
Manuscript Extension Submission Deadline 05 November 2022

Cell death is traditionally divided into programmed cell death (PCD) and necrotic cell death. The balance of cell death, proliferation, and differentiation are critical for maintaining tissue homeostasis throughout life. Except for the canonical form of PCD, such as apoptosis and autophagy, more and more ...

Cell death is traditionally divided into programmed cell death (PCD) and necrotic cell death. The balance of cell death, proliferation, and differentiation are critical for maintaining tissue homeostasis throughout life. Except for the canonical form of PCD, such as apoptosis and autophagy, more and more complex subtypes have been proposed by researchers. Necroptosis, which is usually thought of as type III PCD, was first put forward by Degterev A et al. in 2005. Necroptosis could serve as a substitute mode of cell death that can potentially eliminate cancer cells and prevent tumorigenesis in the absence of apoptosis. Indeed, accumulating evidence indicates that dysregulation of various key necroptotic components may play a role in promoting tumor cell evasion of necroptosis. Pyroptosis was firstly found to be an important mechanism for combating infection. Recently, a study showed that the death of pyroptotic cancer could activate tumor-associated T-cell and dendritic cell (DC) infiltrations.

Furthermore, it was reported that Gasdermin-D (GSDMD) was essential for effector CD8+ T cells to respond to lung cancer. And pyroptosis was also found to be associated with tumor immune microenvironment. Ferroptosis is an iron- and reactive oxygen species (ROS)–a dependent process that may share some homology between species and cross-talk between other cell death pathways. For example, It has been established that two major tumor suppressor proteins, BAP1 and p53, function as important ferroptosis effectors.

In recent years we have seen a rapid development of next-generation sequencing, some non-coding RNAs (ncRNAs), such as microRNA (miRNA), long non-coding RNA (lncRNA), circular RNA (circRNA), and small nucleolar RNA (snoRNA), which were first thought to be transcriptional noise have now been reported to play important roles in many biological processes, including tumorigenesis. However, the role of PCD-related ncRNAs in cancer development is not completely clear. Hence, further research on PCD-related ncRNAs’ effect on the tumor is needed.

The goal of this Research Topic is to uncover a comprehensive summary and systematic analysis of the current understanding of the mechanisms and impact of PCD-related ncRNAs in tumor proliferation, migration, invasion, drug resistance, and immunoregulation. This collection focuses on the underlying crosstalk between programmed cell death processes and ncRNAs in oncogenesis, including competing for endogenous RNA (ceRNA), genetics alteration (RNA interference, mutation), epigenetics regulation (DNA methylation, post-translational modifications of histones). We are also interested in exploring the potential for PCD-related ncRNAs to serve as molecular markers/signatures in predicting the tumor patient’s survival, chemotherapy, radiotherapy, and immunotherapy response.

For this Research Topic, we are interested in Original Research, Review, Mini-Review, Opinion, and Brief Research Report that focuses on the following topics but are not limited to:
• Discovery of PCD-related ncRNAs in tumor development
• The cross-talk between programmed cell death markers/signaling pathway and ncRNAs
• Elucidating mechanisms of PCD-related ncRNAs in proliferation, metastasis, immune escape, or drug resistance in malignant cancers
• Multi-omics analyses of PCD-related ncRNAs
• The potential of EMT-related ncRNAs as new therapeutic targets

Keywords: programmed cell death, ncRNAs, cancer, necroptosis, pyroptosis, ferroptosis


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