c-Myc exerts a protective function through ornithine decarboxylase against cellular insults

Jong Kuk Park, Young Min Chung, Seong Man Kang, Jae Uk Kim, Yun Taik Kim, Hyung Jung Kim, Yeul Hong Kim, Jun Suk Kim, Young Do Yoo

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

c-Myc is known to control cell proliferation and apoptosis, and much effort has been focused on elucidating the mechanisms by which c-Myc works. In this study, we show that c-Myc expression is induced by many cellular insults, including cisplatin, doxorubicin, paclitaxel, 5-flourouracil, H2O2, and radiation, and the enhanced expression of c-Myc protects against cell death caused by these cellular insults through ornithine decarboxylase (ODC) induction. To investigate the cellular protective role of c-Myc, we constructed a stable transfectant of ODC, one of the many transcriptional targets of c-Myc in cells, and found that enhanced expression of ODC inhibited cell death induced by cellular insults such as cisplatin, H2O2, and radiation. We also found that cisplatin activated nuclear factor-κB, and this subsequently induced c-Myc expression, resulting in the blocking of apoptosis through ODC induction. The results herein, therefore, strongly suggest another role for c-Myc in a stress-response function; that is, it promotes cell survival under stressful conditions.

Original languageEnglish
Pages (from-to)1400-1408
Number of pages9
JournalMolecular Pharmacology
Volume62
Issue number6
DOIs
Publication statusPublished - 2002 Dec 1

Fingerprint

Ornithine Decarboxylase
Cisplatin
Cell Death
Radiation
Apoptosis
Doxorubicin
Cell Survival
Cell Proliferation

ASJC Scopus subject areas

  • Pharmacology

Cite this

c-Myc exerts a protective function through ornithine decarboxylase against cellular insults. / Park, Jong Kuk; Chung, Young Min; Kang, Seong Man; Kim, Jae Uk; Kim, Yun Taik; Kim, Hyung Jung; Kim, Yeul Hong; Kim, Jun Suk; Yoo, Young Do.

In: Molecular Pharmacology, Vol. 62, No. 6, 01.12.2002, p. 1400-1408.

Research output: Contribution to journalArticle

Park, Jong Kuk ; Chung, Young Min ; Kang, Seong Man ; Kim, Jae Uk ; Kim, Yun Taik ; Kim, Hyung Jung ; Kim, Yeul Hong ; Kim, Jun Suk ; Yoo, Young Do. / c-Myc exerts a protective function through ornithine decarboxylase against cellular insults. In: Molecular Pharmacology. 2002 ; Vol. 62, No. 6. pp. 1400-1408.
@article{0f70da6c35084a028e04388a98564a55,
title = "c-Myc exerts a protective function through ornithine decarboxylase against cellular insults",
abstract = "c-Myc is known to control cell proliferation and apoptosis, and much effort has been focused on elucidating the mechanisms by which c-Myc works. In this study, we show that c-Myc expression is induced by many cellular insults, including cisplatin, doxorubicin, paclitaxel, 5-flourouracil, H2O2, and radiation, and the enhanced expression of c-Myc protects against cell death caused by these cellular insults through ornithine decarboxylase (ODC) induction. To investigate the cellular protective role of c-Myc, we constructed a stable transfectant of ODC, one of the many transcriptional targets of c-Myc in cells, and found that enhanced expression of ODC inhibited cell death induced by cellular insults such as cisplatin, H2O2, and radiation. We also found that cisplatin activated nuclear factor-κB, and this subsequently induced c-Myc expression, resulting in the blocking of apoptosis through ODC induction. The results herein, therefore, strongly suggest another role for c-Myc in a stress-response function; that is, it promotes cell survival under stressful conditions.",
author = "Park, {Jong Kuk} and Chung, {Young Min} and Kang, {Seong Man} and Kim, {Jae Uk} and Kim, {Yun Taik} and Kim, {Hyung Jung} and Kim, {Yeul Hong} and Kim, {Jun Suk} and Yoo, {Young Do}",
year = "2002",
month = "12",
day = "1",
doi = "10.1124/mol.62.6.1400",
language = "English",
volume = "62",
pages = "1400--1408",
journal = "Molecular Pharmacology",
issn = "0026-895X",
publisher = "American Society for Pharmacology and Experimental Therapeutics",
number = "6",

}

TY - JOUR

T1 - c-Myc exerts a protective function through ornithine decarboxylase against cellular insults

AU - Park, Jong Kuk

AU - Chung, Young Min

AU - Kang, Seong Man

AU - Kim, Jae Uk

AU - Kim, Yun Taik

AU - Kim, Hyung Jung

AU - Kim, Yeul Hong

AU - Kim, Jun Suk

AU - Yoo, Young Do

PY - 2002/12/1

Y1 - 2002/12/1

N2 - c-Myc is known to control cell proliferation and apoptosis, and much effort has been focused on elucidating the mechanisms by which c-Myc works. In this study, we show that c-Myc expression is induced by many cellular insults, including cisplatin, doxorubicin, paclitaxel, 5-flourouracil, H2O2, and radiation, and the enhanced expression of c-Myc protects against cell death caused by these cellular insults through ornithine decarboxylase (ODC) induction. To investigate the cellular protective role of c-Myc, we constructed a stable transfectant of ODC, one of the many transcriptional targets of c-Myc in cells, and found that enhanced expression of ODC inhibited cell death induced by cellular insults such as cisplatin, H2O2, and radiation. We also found that cisplatin activated nuclear factor-κB, and this subsequently induced c-Myc expression, resulting in the blocking of apoptosis through ODC induction. The results herein, therefore, strongly suggest another role for c-Myc in a stress-response function; that is, it promotes cell survival under stressful conditions.

AB - c-Myc is known to control cell proliferation and apoptosis, and much effort has been focused on elucidating the mechanisms by which c-Myc works. In this study, we show that c-Myc expression is induced by many cellular insults, including cisplatin, doxorubicin, paclitaxel, 5-flourouracil, H2O2, and radiation, and the enhanced expression of c-Myc protects against cell death caused by these cellular insults through ornithine decarboxylase (ODC) induction. To investigate the cellular protective role of c-Myc, we constructed a stable transfectant of ODC, one of the many transcriptional targets of c-Myc in cells, and found that enhanced expression of ODC inhibited cell death induced by cellular insults such as cisplatin, H2O2, and radiation. We also found that cisplatin activated nuclear factor-κB, and this subsequently induced c-Myc expression, resulting in the blocking of apoptosis through ODC induction. The results herein, therefore, strongly suggest another role for c-Myc in a stress-response function; that is, it promotes cell survival under stressful conditions.

UR - http://www.scopus.com/inward/record.url?scp=0036892306&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036892306&partnerID=8YFLogxK

U2 - 10.1124/mol.62.6.1400

DO - 10.1124/mol.62.6.1400

M3 - Article

VL - 62

SP - 1400

EP - 1408

JO - Molecular Pharmacology

JF - Molecular Pharmacology

SN - 0026-895X

IS - 6

ER -