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First, recent studies have found that metabolic reprogramming has occurred in human leukocytes.
Our study showed that metabolic reprogramming has occurred in whole blood.
In just the last ten years, the significance of metabolic reprogramming has led to its inclusion with the classic hallmarks of cancer (Hanahan and Weinberg, 2011).
While novel within the critical care context, our finding that glycolysis participates in metabolic reprogramming has been well observed in oncology [16].
Therefore, metabolic reprogramming has become an important area of research to better understand disease at the cellular level, as well as to identify targets for treatment.
Recently, metabolic reprogramming has been recognized as a hallmark of cancer [ 4– 6].
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Whilst the molecular underpinnings of this metabolic reprogramming have been described, its role in tumor progression is still under investigation.
However, it is only recently that the mechanisms responsible for this metabolic reprogramming have been elucidated in more detail.
Indeed, abnormal cell cycle progression, defective apoptosis, and metabolic reprogramming have been implicated as key mechanisms of OVCA chemoresistance (Takahashi et al, 2005; Hajra et al, 2008; Etemadmoghadam et al, 2009; Montopoli et al, 2011).
In addition to metabolic reprogramming, PKM2 has also been demonstrated to directly regulate gene expression and subsequent cell cycle progression [ 6].
In spite of this, however, how it works and what this cellular metabolic reprogramming does have long remained unclear [ 2].
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