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Metabolic deregulation is an established hallmark of cancer. Although it is accepted that most cancer cells consume increased amounts of glucose and amino acids to satisfy energy, and biosynthesis demands for rapid proliferation, a complex and heterogeneous metabolic scenario has been described depending on ...

Metabolic deregulation is an established hallmark of cancer. Although it is accepted that most cancer cells consume increased amounts of glucose and amino acids to satisfy energy, and biosynthesis demands for rapid proliferation, a complex and heterogeneous metabolic scenario has been described depending on numerous variables including tumor type and stage. Importantly, the metabolic phenotype of a given tumor is largely influenced not only by the local microenvironment but also by therapeutic interventions.

Despite Warburg reporting that, even in the presence of oxygen, cancer cells show increased glycolysis funneling of only a small fraction of glucose for oxidative phosphorylation (OXPHOS), whether such metabolic deregulation is a requisite for malignant transformation, tumor progression, and resistance to treatment remains a matter of debate.

This Research Topic aims to discuss the complex aspects of metabolic deregulation in cancer cells including (but not limited to):
-metabolic reprogramming associated with cancer phenotype, either dependent or independent of oncogene or oncosuppressor addiction;
-metabolic crosstalk between the cell types that are present in the tumor microenvironment; -metabolites that could be implicated in tumor initiation and progression with a non-metabolic role (e.g. involved in epigenetic reprogramming or signaling pathways activation).

Importantly, reports discussing potential metabolic targeting approaches, either alone or in combination with the standard therapeutic regimens, will be appreciated in this Research Topic. Authors are welcome to submit original research or review articles to provide the readers with up-to-date knowledge of the role of metabolic reprogramming in supporting and driving all the aspects of cancer biology.

Keywords: cancer, metabolism, mitochondria, therapy resistance, metabolic reprogramming


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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