AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability

Bum Joon Park; Young Sun Oh; Seung Yong Park; So Jung Choi; Cornelia Rudolph; Brigitte Schlegelberger; Sunghoon Kim

doi:10.1158/0008-5472.CAN-05-3740

AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability

Bum Joon Park, Young Sun Oh, Seung Yong Park, So Jung Choi, Cornelia Rudolph, Brigitte Schlegelberger, Sunghoon Kim

Department of Pharmacy

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

53 Citations (Scopus)

Abstract

AIMP3 (previously known as p18) was shown to up-regulate p53 in response to DNA damage. Here, we show that AIMP3 couples oncogenic stresses to p53 activation to prevent cell transformation. Growth factor- or Ras-dependent induction of p53 was blocked by single allelic loss of AIMP3 as well as by suppression of AIMP3. AIMP3 heterozygous cells became susceptible to cell transformation induced by oncogenes such as Ras or Myc alone. The transformed AIMP3^+/- cells showed severe abnormality in cell division and chromosomal structure. Thus, AIMP3 plays crucial roles in p53-mediated tumor-suppressive response against oncogenic stresses via differential activation of ATM and ATR, and in the maintenance of genomic stability.

Original language	English
Pages (from-to)	6913-6918
Number of pages	6
Journal	Cancer Research
Volume	66
Issue number	14
DOIs	https://doi.org/10.1158/0008-5472.CAN-05-3740
Publication status	Published - 2006 Jul 15

All Science Journal Classification (ASJC) codes

Oncology
Cancer Research

UN SDGs

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

Access to Document

10.1158/0008-5472.CAN-05-3740

Cite this

@article{2adf6711e2124a47a9756151cee566d9,

title = "AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability",

abstract = "AIMP3 (previously known as p18) was shown to up-regulate p53 in response to DNA damage. Here, we show that AIMP3 couples oncogenic stresses to p53 activation to prevent cell transformation. Growth factor- or Ras-dependent induction of p53 was blocked by single allelic loss of AIMP3 as well as by suppression of AIMP3. AIMP3 heterozygous cells became susceptible to cell transformation induced by oncogenes such as Ras or Myc alone. The transformed AIMP3+/- cells showed severe abnormality in cell division and chromosomal structure. Thus, AIMP3 plays crucial roles in p53-mediated tumor-suppressive response against oncogenic stresses via differential activation of ATM and ATR, and in the maintenance of genomic stability.",

author = "Park, {Bum Joon} and Oh, {Young Sun} and Park, {Seung Yong} and Choi, {So Jung} and Cornelia Rudolph and Brigitte Schlegelberger and Sunghoon Kim",

year = "2006",

month = jul,

day = "15",

doi = "10.1158/0008-5472.CAN-05-3740",

language = "English",

volume = "66",

pages = "6913--6918",

journal = "Cancer Research",

issn = "0008-5472",

number = "14",

}

TY - JOUR

T1 - AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability

AU - Park, Bum Joon

AU - Oh, Young Sun

AU - Park, Seung Yong

AU - Choi, So Jung

AU - Rudolph, Cornelia

AU - Schlegelberger, Brigitte

AU - Kim, Sunghoon

PY - 2006/7/15

Y1 - 2006/7/15

N2 - AIMP3 (previously known as p18) was shown to up-regulate p53 in response to DNA damage. Here, we show that AIMP3 couples oncogenic stresses to p53 activation to prevent cell transformation. Growth factor- or Ras-dependent induction of p53 was blocked by single allelic loss of AIMP3 as well as by suppression of AIMP3. AIMP3 heterozygous cells became susceptible to cell transformation induced by oncogenes such as Ras or Myc alone. The transformed AIMP3+/- cells showed severe abnormality in cell division and chromosomal structure. Thus, AIMP3 plays crucial roles in p53-mediated tumor-suppressive response against oncogenic stresses via differential activation of ATM and ATR, and in the maintenance of genomic stability.

AB - AIMP3 (previously known as p18) was shown to up-regulate p53 in response to DNA damage. Here, we show that AIMP3 couples oncogenic stresses to p53 activation to prevent cell transformation. Growth factor- or Ras-dependent induction of p53 was blocked by single allelic loss of AIMP3 as well as by suppression of AIMP3. AIMP3 heterozygous cells became susceptible to cell transformation induced by oncogenes such as Ras or Myc alone. The transformed AIMP3+/- cells showed severe abnormality in cell division and chromosomal structure. Thus, AIMP3 plays crucial roles in p53-mediated tumor-suppressive response against oncogenic stresses via differential activation of ATM and ATR, and in the maintenance of genomic stability.

UR - http://www.scopus.com/inward/record.url?scp=33746872495&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33746872495&partnerID=8YFLogxK

U2 - 10.1158/0008-5472.CAN-05-3740

DO - 10.1158/0008-5472.CAN-05-3740

M3 - Article

C2 - 16849534

AN - SCOPUS:33746872495

SN - 0008-5472

VL - 66

SP - 6913

EP - 6918

JO - Cancer Research

JF - Cancer Research

IS - 14

ER -

AIMP3 haploinsufficiency disrupts oncogene-induced p53 activation and genomic stability

Abstract

All Science Journal Classification (ASJC) codes

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this