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Chicken or the egg: Warburg effect and mitochondrial dysfunction.

Senyilmaz D, Teleman AA - F1000Prime Rep (2015)

Bottom Line: However, this hypothesis did not convince every scientist in the field.Some believed the opposite: the reduction in mitochondrial activity is a result of increased glycolysis.This discrepancy of opinions is ongoing.

View Article: PubMed Central - PubMed

Affiliation: German Cancer Research Center (DKFZ) Heidelberg Germany.

ABSTRACT
Compared with normal cells, cancer cells show alterations in many cellular processes, including energy metabolism. Studies on cancer metabolism started with Otto Warburg's observation at the beginning of the last century. According to Warburg, cancer cells rely on glycolysis more than mitochondrial respiration for energy production. Considering that glycolysis yields much less energy compared with mitochondrial respiration, Warburg hypothesized that mitochondria must be dysfunctional and this is the initiating factor for cancer formation. However, this hypothesis did not convince every scientist in the field. Some believed the opposite: the reduction in mitochondrial activity is a result of increased glycolysis. This discrepancy of opinions is ongoing. In this review, we will discuss the alterations in glycolysis, pyruvate metabolism, and the Krebs cycle in cancer cells and focus on cause and consequence.

No MeSH data available.


Related in: MedlinePlus

In cancer cells, reduction of pyruvate to lactate and its secretion is favored rather than pyruvate entry into mitochondria and the Krebs cycleDCA, dichloroacetate; HIF1, hypoxia-induced factor 1; LDHA, lactate dehydrogenase A; MCT4, monocarboxylate transporter 4; MPC, mitochondrial pyruvate carrier; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; TCA, tricarboxylic acid.
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fig-002: In cancer cells, reduction of pyruvate to lactate and its secretion is favored rather than pyruvate entry into mitochondria and the Krebs cycleDCA, dichloroacetate; HIF1, hypoxia-induced factor 1; LDHA, lactate dehydrogenase A; MCT4, monocarboxylate transporter 4; MPC, mitochondrial pyruvate carrier; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; TCA, tricarboxylic acid.

Mentions: Pyruvate is the critical node where the flux of glucose-derived carbons is determined, either toward lactate which is usually secreted or into mitochondria (Figure 2). As Warburg observed, cancer cells metabolize pyruvate by aerobic glycolysis and produce lactate. Here, we will discuss the mechanisms of aerobic glycolysis induction which do not necessarily stem from dysfunctional mitochondria, which would have pleased Weinhouse.


Chicken or the egg: Warburg effect and mitochondrial dysfunction.

Senyilmaz D, Teleman AA - F1000Prime Rep (2015)

In cancer cells, reduction of pyruvate to lactate and its secretion is favored rather than pyruvate entry into mitochondria and the Krebs cycleDCA, dichloroacetate; HIF1, hypoxia-induced factor 1; LDHA, lactate dehydrogenase A; MCT4, monocarboxylate transporter 4; MPC, mitochondrial pyruvate carrier; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; TCA, tricarboxylic acid.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4447048&req=5

fig-002: In cancer cells, reduction of pyruvate to lactate and its secretion is favored rather than pyruvate entry into mitochondria and the Krebs cycleDCA, dichloroacetate; HIF1, hypoxia-induced factor 1; LDHA, lactate dehydrogenase A; MCT4, monocarboxylate transporter 4; MPC, mitochondrial pyruvate carrier; PDH, pyruvate dehydrogenase; PDK, pyruvate dehydrogenase kinase; TCA, tricarboxylic acid.
Mentions: Pyruvate is the critical node where the flux of glucose-derived carbons is determined, either toward lactate which is usually secreted or into mitochondria (Figure 2). As Warburg observed, cancer cells metabolize pyruvate by aerobic glycolysis and produce lactate. Here, we will discuss the mechanisms of aerobic glycolysis induction which do not necessarily stem from dysfunctional mitochondria, which would have pleased Weinhouse.

Bottom Line: However, this hypothesis did not convince every scientist in the field.Some believed the opposite: the reduction in mitochondrial activity is a result of increased glycolysis.This discrepancy of opinions is ongoing.

View Article: PubMed Central - PubMed

Affiliation: German Cancer Research Center (DKFZ) Heidelberg Germany.

ABSTRACT
Compared with normal cells, cancer cells show alterations in many cellular processes, including energy metabolism. Studies on cancer metabolism started with Otto Warburg's observation at the beginning of the last century. According to Warburg, cancer cells rely on glycolysis more than mitochondrial respiration for energy production. Considering that glycolysis yields much less energy compared with mitochondrial respiration, Warburg hypothesized that mitochondria must be dysfunctional and this is the initiating factor for cancer formation. However, this hypothesis did not convince every scientist in the field. Some believed the opposite: the reduction in mitochondrial activity is a result of increased glycolysis. This discrepancy of opinions is ongoing. In this review, we will discuss the alterations in glycolysis, pyruvate metabolism, and the Krebs cycle in cancer cells and focus on cause and consequence.

No MeSH data available.


Related in: MedlinePlus