P53 regulates glucose metabolism by miR-34a

Hwa Ryeon Kim; Jae Seok Roe; Ji Eun Lee; Eun Jung Cho; Hong Duk Youn

doi:10.1016/j.bbrc.2013.06.043

P53 regulates glucose metabolism by miR-34a

Hwa Ryeon Kim, Jae Seok Roe, Ji Eun Lee, Eun Jung Cho, Hong Duk Youn

Department of Biochemistry

Research output: Contribution to journal › Article › peer-review

76 Citations (Scopus)

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	https://doi.org/10.1016/j.bbrc.2013.06.043
Publication status	Published - 2013 Jul 26

Bibliographical note

Funding Information:
This work was supported by National Research Foundation of Korea (NRF) grants funded by the Korea government (MSIP) [National Creative Research Laboratory Program ( 2012R1A3A2048767 ), the Mid-Career Research Program, the National Research Foundation of Korea ( NRF-2007-0056786 & NRF-2010-0007643 ), and the World Class University Program of the MEST and the NRF ( R31-2008-000-10103-0 )], and partly from the National R&D Program for Cancer Control, Ministry of Health & Welfare ( 0720460 ) to H.D.Y.

All Science Journal Classification (ASJC) codes

Biophysics
Biochemistry
Molecular Biology
Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1016/j.bbrc.2013.06.043

Cite this

@article{fabb9ccc43d0473291ec6ffd76fc64f7,

title = "P53 regulates glucose metabolism by miR-34a",

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.",

author = "Kim, {Hwa Ryeon} and Roe, {Jae Seok} and Lee, {Ji Eun} and Cho, {Eun Jung} and Youn, {Hong Duk}",

note = "Funding Information: This work was supported by National Research Foundation of Korea (NRF) grants funded by the Korea government (MSIP) [National Creative Research Laboratory Program ( 2012R1A3A2048767 ), the Mid-Career Research Program, the National Research Foundation of Korea ( NRF-2007-0056786 & NRF-2010-0007643 ), and the World Class University Program of the MEST and the NRF ( R31-2008-000-10103-0 )], and partly from the National R&D Program for Cancer Control, Ministry of Health & Welfare ( 0720460 ) to H.D.Y. ",

year = "2013",

month = jul,

day = "26",

doi = "10.1016/j.bbrc.2013.06.043",

language = "English",

volume = "437",

pages = "225--231",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "2",

}

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

N1 - Funding Information: This work was supported by National Research Foundation of Korea (NRF) grants funded by the Korea government (MSIP) [National Creative Research Laboratory Program ( 2012R1A3A2048767 ), the Mid-Career Research Program, the National Research Foundation of Korea ( NRF-2007-0056786 & NRF-2010-0007643 ), and the World Class University Program of the MEST and the NRF ( R31-2008-000-10103-0 )], and partly from the National R&D Program for Cancer Control, Ministry of Health & Welfare ( 0720460 ) to H.D.Y.

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 -

P53 regulates glucose metabolism by miR-34a

Abstract

Bibliographical note

All Science Journal Classification (ASJC) codes

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this