About this Research Topic
Epithelial-mesenchymal plasticity (EMP) is the ability of cells to transit between epithelial and mesenchymal states through epithelial-to-mesenchymal transition (EMT) and its reverse process mesenchymal-to-epithelial transition (MET). EMT and MET are two fundamental biological processes playing critical roles during embryonic development and in disease. In cancer, epithelial-mesenchymal plasticity (EMP) has been shown to promote tumor invasion and metastasis; EMP facilitates tumor metastasis, cancer stem cell generation and maintenance, and resistance to therapeutics. Due to the positive association between EMT and metastasis, it has been the primary focus of cancer research for decades. Only in recent years, MET research has become mainstream. This difference of interest created a relatively comprehensive understanding of EMT biology and its regulation, extending to applications for therapeutic development. On the other hand, a similar understanding of MET is lagging.
Although the area of EMT research rapidly expanded in the last two decades, we are still far from understanding the biological mechanism and pathological contribution of EMP in cancer. One reason is the scarcity of data on MET, which was neglected, probably, assuming the reversal of EMT would simply mean the exact opposite of the whole process. Recent evidence shows that distinct regulatory cues govern MET at the transcriptional and epigenetic levels. Several transcription factors, such as Grhl2/3, Ovol2 and Klf4, have been implicated in the regulation of MET. More studies on the regulation of MET are essential to better understand not only the developmental processes but also to improve the current views on metastasis. Such studies will also advance our understanding of EMP and its relevance during different stages of tumor initiation, progression, metastasis, and resistance to therapeutics. The pleiotropic functions of EMT/MET associated with cell stemness, metastasis, and therapy resistance, highlight great therapeutic opportunities. Targeting key transcriptional or epigenetic control mechanisms of cellular plasticity might interfere with or even freeze EMP and thereby prevent the flexible interconversion of epithelial-mesenchymal cancer cell states needed for metastasis while at the same time making the cancer cells more accessible for various therapeutic approaches.
This research topic welcomes research articles and reviews focused on deciphering the regulatory mechanisms of EMT, MET, and the role of EMP in cancer progression, metastasis, and therapy resistance. Authors can contribute to this topic based on the following specific themes:
• Transcriptional regulation of MET
• Epigenetics of MET (non-coding RNAs, DNA methylation, Histone variants)
• Overview of canonical and non-canonical EMT pathways during cancer progression
• Defining hybrid E/M state in EMP and its clinical implications
• Changing tumor microenvironment during EMP
• EMP phenotypes and their clinical relevance
• EMP in regulating stemness of cancer stem cells
• Role EMP plays in defining cancer immunotherapy responses
• Advanced models for studying EMP
We accept different article types including Mini-Reviews, Brief Research Reports and Perspectives. A full list of accepted article types, including descriptions, can be found at this link.
Please note: studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
Although the area of EMT research rapidly expanded in the last two decades, we are still far from understanding the biological mechanism and pathological contribution of EMP in cancer. One reason is the scarcity of data on MET, which was neglected, probably, assuming the reversal of EMT would simply mean the exact opposite of the whole process. Recent evidence shows that distinct regulatory cues govern MET at the transcriptional and epigenetic levels. Several transcription factors, such as Grhl2/3, Ovol2 and Klf4, have been implicated in the regulation of MET. More studies on the regulation of MET are essential to better understand not only the developmental processes but also to improve the current views on metastasis. Such studies will also advance our understanding of EMP and its relevance during different stages of tumor initiation, progression, metastasis, and resistance to therapeutics. The pleiotropic functions of EMT/MET associated with cell stemness, metastasis, and therapy resistance, highlight great therapeutic opportunities. Targeting key transcriptional or epigenetic control mechanisms of cellular plasticity might interfere with or even freeze EMP and thereby prevent the flexible interconversion of epithelial-mesenchymal cancer cell states needed for metastasis while at the same time making the cancer cells more accessible for various therapeutic approaches.
This research topic welcomes research articles and reviews focused on deciphering the regulatory mechanisms of EMT, MET, and the role of EMP in cancer progression, metastasis, and therapy resistance. Authors can contribute to this topic based on the following specific themes:
• Transcriptional regulation of MET
• Epigenetics of MET (non-coding RNAs, DNA methylation, Histone variants)
• Overview of canonical and non-canonical EMT pathways during cancer progression
• Defining hybrid E/M state in EMP and its clinical implications
• Changing tumor microenvironment during EMP
• EMP phenotypes and their clinical relevance
• EMP in regulating stemness of cancer stem cells
• Role EMP plays in defining cancer immunotherapy responses
• Advanced models for studying EMP
We accept different article types including Mini-Reviews, Brief Research Reports and Perspectives. A full list of accepted article types, including descriptions, can be found at this link.
Please note: studies consisting solely of bioinformatic investigation of publicly available genomic/transcriptomic/proteomic data do not fall within the scope of the section unless they are expanded and provide significant biological or mechanistic insight into the process being studied.
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.
