It would seem logical to assume that hypoxia is what
drives tumor cells to fuel glucose in a nonoxidative
‘glucose to lactate’ pathway. However, it is currently
believed that the glycolytic switch is acquired very early
in carcinogenesis even before tumors experience hypoxia
[7]. For example, lung cancers and leukemic cells, which
are growing in the presence of oxygen, fuel glucose into
the aerobic glycolysis pathway [14,15]. Consequently, the
fact that, even in normoxic conditions, many tumors use
aerobic glycolysis for their metabolic requirements
indicates that the Warburg effect has functions that are
not solely limited to hypoxia adaptation. We will come
later to possible reasons why tumors turn on aerobic
glycolysis but let us first discuss other responses induced
by hypoxia in tumor cells.
It would seem logical to assume that hypoxia is what
drives tumor cells to fuel glucose in a nonoxidative
‘glucose to lactate’ pathway. However, it is currently
believed that the glycolytic switch is acquired very early
in carcinogenesis even before tumors experience hypoxia
[7]. For example, lung cancers and leukemic cells, which
are growing in the presence of oxygen, fuel glucose into
the aerobic glycolysis pathway [14,15]. Consequently, the
fact that, even in normoxic conditions, many tumors use
aerobic glycolysis for their metabolic requirements
indicates that the Warburg effect has functions that are
not solely limited to hypoxia adaptation. We will come
later to possible reasons why tumors turn on aerobic
glycolysis but let us first discuss other responses induced
by hypoxia in tumor cells.
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