Research Topic

Oncogenic RAS-dependent Reprogramming of Cellular Plasticity

About this Research Topic

RAS proteins are the major onco-proteins with neoplastic potential widespread in various types of human cancers. Over the years it has been discovered that all four RAS isoforms (H-RAS, K-RAS4A, K-RAS4B and N-RAS) play a critical role in carcinogenesis leading to the development of characteristic features of cancer cells which to date are the major concern for antineoplastic therapy.

RAS proteins are activated by receptor tyrosine kinases and transduce extracellular signals to the nucleus, initiating multiple and compartmentalized signaling cascades involved in the regulation of cell growth and differentiation. The highest mutation frequency of these proto-oncogenes and the consequent incessant RAS activation are observed in cancers with few therapeutic options, allowing the maintenance of tumor survival, proliferation and invasion. The hyperactive RAS proteins lead to dysregulation of major intracellular signaling cascades favoring the arise of cancer hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, metabolic reprogramming, genomic instability and remodeling of the tumor microenvironment. The ensemble of all these interconnected reactions is central to cellular plasticity, resulting in a severe malignancy and resistance to therapy.

More than 30 years after its discovery, RAS has become a prime target of research. The dependency of tumor cells on its oncogenic activity strongly suggests that targeting oncogenic RAS or its effectors can be a good therapeutic approach for cancer eradication and a perfect instrument to fully understand RAS signaling pathways in cancer.

In this Research Topic we welcome original research and review articles that will contribute to the understanding of signaling pathways originating from oncogenic RAS. The implications of these signaling networks in the establishment and maintenance of cancer hallmarks will be of particular interest to our readers. Potential topics include, but are not limited to:
• Metabolic reprogramming and homeostatic adaptation
• Tumor-promoting inflammation
• Altered redox balance
• Proteotoxic stress
• Sustained angiogenesis
• Chemoresistance
• Tissue invasion and metastasis
• Recent developments related to RAS pharmacological targeting
• Novel approaches to target RAS-driven tumors


Keywords: Oncogenic RAS, cancer hallmarks, therapy resistance, cellular plasticity, Oncogenesis


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.

RAS proteins are the major onco-proteins with neoplastic potential widespread in various types of human cancers. Over the years it has been discovered that all four RAS isoforms (H-RAS, K-RAS4A, K-RAS4B and N-RAS) play a critical role in carcinogenesis leading to the development of characteristic features of cancer cells which to date are the major concern for antineoplastic therapy.

RAS proteins are activated by receptor tyrosine kinases and transduce extracellular signals to the nucleus, initiating multiple and compartmentalized signaling cascades involved in the regulation of cell growth and differentiation. The highest mutation frequency of these proto-oncogenes and the consequent incessant RAS activation are observed in cancers with few therapeutic options, allowing the maintenance of tumor survival, proliferation and invasion. The hyperactive RAS proteins lead to dysregulation of major intracellular signaling cascades favoring the arise of cancer hallmarks, including sustained proliferative signaling, evasion of growth suppressors, resistance to cell death, metabolic reprogramming, genomic instability and remodeling of the tumor microenvironment. The ensemble of all these interconnected reactions is central to cellular plasticity, resulting in a severe malignancy and resistance to therapy.

More than 30 years after its discovery, RAS has become a prime target of research. The dependency of tumor cells on its oncogenic activity strongly suggests that targeting oncogenic RAS or its effectors can be a good therapeutic approach for cancer eradication and a perfect instrument to fully understand RAS signaling pathways in cancer.

In this Research Topic we welcome original research and review articles that will contribute to the understanding of signaling pathways originating from oncogenic RAS. The implications of these signaling networks in the establishment and maintenance of cancer hallmarks will be of particular interest to our readers. Potential topics include, but are not limited to:
• Metabolic reprogramming and homeostatic adaptation
• Tumor-promoting inflammation
• Altered redox balance
• Proteotoxic stress
• Sustained angiogenesis
• Chemoresistance
• Tissue invasion and metastasis
• Recent developments related to RAS pharmacological targeting
• Novel approaches to target RAS-driven tumors


Keywords: Oncogenic RAS, cancer hallmarks, therapy resistance, cellular plasticity, Oncogenesis


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.

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Submission Deadlines

19 July 2019 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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Topic Editors

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Submission Deadlines

19 July 2019 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

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