Abstract
Cancer cells rely mainly on glycolysis rather than mitochondrial respiration for energy production, which is called the Warburg effect. p53 mutations are observed in about half of cancer cases, and p53 controls the cell cycle and cell death in response to cellular stressors. p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism. Here, we demonstrated metabolic changes in cancer that occurred through p53. We found that p53-inducible microRNA-34a (miR-34a) repressed glycolytic enzymes (hexokinase 1, hexokinase 2, glucose-6-phosphate isomerase), and pyruvate dehydrogenase kinase 1. Treatment with an anti-miR-34a inhibitor relieved the decreased expression in these enzymes following DNA damage. miR-34a-mediated inhibition of these enzymes resulted in repressed glycolysis and enhanced mitochondrial respiration. The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism.
| Original language | English |
|---|---|
| Pages (from-to) | 225-231 |
| Number of pages | 7 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 437 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2013 Jul 26 |
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All Science Journal Classification (ASJC) codes
- Biophysics
- Biochemistry
- Molecular Biology
- Cell Biology
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P53 regulates glucose metabolism by miR-34a. / Kim, Hwa Ryeon; Roe, Jae Seok; Lee, Ji Eun; Cho, Eun Jung; Youn, Hong Duk.
In: Biochemical and Biophysical Research Communications, Vol. 437, No. 2, 26.07.2013, p. 225-231.Research output: Contribution to journal › Article
TY - JOUR
T1 - P53 regulates glucose metabolism by miR-34a
AU - Kim, Hwa Ryeon
AU - Roe, Jae Seok
AU - Lee, Ji Eun
AU - Cho, Eun Jung
AU - Youn, Hong Duk
PY - 2013/7/26
Y1 - 2013/7/26
N2 - Cancer cells rely mainly on glycolysis rather than mitochondrial respiration for energy production, which is called the Warburg effect. p53 mutations are observed in about half of cancer cases, and p53 controls the cell cycle and cell death in response to cellular stressors. p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism. Here, we demonstrated metabolic changes in cancer that occurred through p53. We found that p53-inducible microRNA-34a (miR-34a) repressed glycolytic enzymes (hexokinase 1, hexokinase 2, glucose-6-phosphate isomerase), and pyruvate dehydrogenase kinase 1. Treatment with an anti-miR-34a inhibitor relieved the decreased expression in these enzymes following DNA damage. miR-34a-mediated inhibition of these enzymes resulted in repressed glycolysis and enhanced mitochondrial respiration. The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism.
AB - Cancer cells rely mainly on glycolysis rather than mitochondrial respiration for energy production, which is called the Warburg effect. p53 mutations are observed in about half of cancer cases, and p53 controls the cell cycle and cell death in response to cellular stressors. p53 has been emphasized as a metabolic regulator involved in glucose, glutamine, and purine metabolism. Here, we demonstrated metabolic changes in cancer that occurred through p53. We found that p53-inducible microRNA-34a (miR-34a) repressed glycolytic enzymes (hexokinase 1, hexokinase 2, glucose-6-phosphate isomerase), and pyruvate dehydrogenase kinase 1. Treatment with an anti-miR-34a inhibitor relieved the decreased expression in these enzymes following DNA damage. miR-34a-mediated inhibition of these enzymes resulted in repressed glycolysis and enhanced mitochondrial respiration. The results suggest that p53 has a miR-34a-dependent integrated mechanism to regulate glucose metabolism.
UR - http://www.scopus.com/inward/record.url?scp=84880713203&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84880713203&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2013.06.043
DO - 10.1016/j.bbrc.2013.06.043
M3 - Article
C2 - 23796712
AN - SCOPUS:84880713203
VL - 437
SP - 225
EP - 231
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -