open access

Vol 63, No 2 (2013)
Review articles
Published online: 2013-06-10
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How tumour cells respirate?

Anna Gasińska, Anna Janecka, Agnieszka Adamczyk, Dorota Słonina
Nowotwory. Journal of Oncology 2013;63(2):124-131.

open access

Vol 63, No 2 (2013)
Review articles
Published online: 2013-06-10

Abstract

Otto Warburg at the beginning of the 20th century suggested that cancer cells exhibit diff erent metabolism than normal
cells. He demonstrated that tumour cells prefer aerobic glycolisis rather than oxidative respiration as for normal
cells. They convert large amounts of glucose to lactate in the process of glycolysis, and even in the presence of oxygen.
The phenomenon is known as the Warburg eff ect or aerobic glycolysis. The biochemist hypothesized that the cause of
this is mitochondrial damage in tumour cells. The reason why cells undergo the Warburg eff ect is still poorly understood.
However it is known that many proliferating cells, also malignant cells, show increased uptake of glucose and
restriction of oxidative phosphorylation. This metabolic pathway facilitates high levels of lactate production, even
in the presence of oxygen. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular diff erentiation. These changes facilitate the process of oncogenesis and cell growth.
The pyruvate kinase (PK), a glycolitic enzyme is replaced by isoform of PKM2 which facilitates aerobic glycolisis
in cancer cells. PKM2 is also a regulator of cellular anti-oxidative metabolism which promotes cancer growth by
activating pentose phosphate pathway, maintaining the balance of redox equivalents and activating antioxidant
defence system. Recently there has been proposed a new model of cancer metabolism, which has been proved
experimentally, termed reverse Warburg eff ect. This model explains the role of aerobic glycolysis and lactate production
in fueling tumour growth. This model assumes metabolic cooperation between stromal fi broblasts and
tumour cells, and that cancer cells perform oxidative respiration. In activated fi broblasts, oxidative stress in the
tumour microenvironment leads to authophagy, mitophagy and aerobic glycolysis, which delivers high-energetic
intermediates such as lactate, ketones and glutamine to tumour cells that fuel the anabolic growth. Tumour cells
due to delivered nutrients can lead anabolic metabolism and produce high amounts of ATP what facilitates tumour
growth, development and progression.

Abstract

Otto Warburg at the beginning of the 20th century suggested that cancer cells exhibit diff erent metabolism than normal
cells. He demonstrated that tumour cells prefer aerobic glycolisis rather than oxidative respiration as for normal
cells. They convert large amounts of glucose to lactate in the process of glycolysis, and even in the presence of oxygen.
The phenomenon is known as the Warburg eff ect or aerobic glycolysis. The biochemist hypothesized that the cause of
this is mitochondrial damage in tumour cells. The reason why cells undergo the Warburg eff ect is still poorly understood.
However it is known that many proliferating cells, also malignant cells, show increased uptake of glucose and
restriction of oxidative phosphorylation. This metabolic pathway facilitates high levels of lactate production, even
in the presence of oxygen. Recent evidence suggests that metabolites themselves can be oncogenic by altering cell signaling and blocking cellular diff erentiation. These changes facilitate the process of oncogenesis and cell growth.
The pyruvate kinase (PK), a glycolitic enzyme is replaced by isoform of PKM2 which facilitates aerobic glycolisis
in cancer cells. PKM2 is also a regulator of cellular anti-oxidative metabolism which promotes cancer growth by
activating pentose phosphate pathway, maintaining the balance of redox equivalents and activating antioxidant
defence system. Recently there has been proposed a new model of cancer metabolism, which has been proved
experimentally, termed reverse Warburg eff ect. This model explains the role of aerobic glycolysis and lactate production
in fueling tumour growth. This model assumes metabolic cooperation between stromal fi broblasts and
tumour cells, and that cancer cells perform oxidative respiration. In activated fi broblasts, oxidative stress in the
tumour microenvironment leads to authophagy, mitophagy and aerobic glycolysis, which delivers high-energetic
intermediates such as lactate, ketones and glutamine to tumour cells that fuel the anabolic growth. Tumour cells
due to delivered nutrients can lead anabolic metabolism and produce high amounts of ATP what facilitates tumour
growth, development and progression.
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About this article
Title

How tumour cells respirate?

Journal

Nowotwory. Journal of Oncology

Issue

Vol 63, No 2 (2013)

Pages

124-131

Published online

2013-06-10

Bibliographic record

Nowotwory. Journal of Oncology 2013;63(2):124-131.

Authors

Anna Gasińska
Anna Janecka
Agnieszka Adamczyk
Dorota Słonina

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