Identification of radiation-specific responses from gene expression profile

Woong Yang Park; Chang Il Hwang; Chang Nim Im; Min Ji Kang; Jang Hee Woo; Ju Hoon Kim; Yon Su Kim; Ju Han Kim; Ho Kim; Kyung A. Kim; Hyung Jin Yu; Sue Jae Lee; Yun Sil Lee; Jeong Sun Seo

doi:10.1038/sj.onc.1205977

Identification of radiation-specific responses from gene expression profile

Woong Yang Park, Chang Il Hwang, Chang Nim Im, Min Ji Kang, Jang Hee Woo, Ju Hoon Kim, Yon Su Kim, Ju Han Kim, Ho Kim, Kyung A. Kim, Hyung Jin Yu, Sue Jae Lee, Yun Sil Lee, Jeong Sun Seo

Department of Pharmaceutical Sciences

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

104 Scopus citations

Abstract

The responses to ionizing radiation (IR) in tumors are dependent on cellular context. We investigated radiation-related expression patterns in Jurkat T cells with nonsense mutation in p53 using cDNA microarray. Expression of 2400 genes in γ-irradiated cells was distinct from other stimulations like anti-CD3, phetohemagglutinin (PHA) and concanavalin A (ConA) in unsupervised clustering analysis. Among them, 384 genes were selected for their IR-specific changes to make 'RadChip'. In spite of p53 status, every type of cells showed similar patterns in expression of these genes upon γ-radiation. Moreover, radiation-induced responses were clearly separated from the responses to other genotoxic stress like UV radiation, cisplatin and doxorubicin. We focused on two IR-related genes, phospholipase Cγ2 (PLCG2) and cytosolic epoxide hydrolase (EPHX2), which were increased at 12 h after γ-radiation in RT-PCR. TPCK could suppress the induction of these two genes in either of Jurkat T cells and PBMCs, which might suggest the transcriptional regulation of PLCG2 and EPHX2 by NF-κB upon γ-radiation. From these results, we could identify the IR-specific genes from expression profiling, which can be used as radiation biomarkers to screen radiation exposure as well as probing the mechanism of cellular responses to ionizing radiation.

Original language	English
Pages (from-to)	8521-8528
Number of pages	8
Journal	Oncogene
Volume	21
Issue number	55
DOIs	https://doi.org/10.1038/sj.onc.1205977
State	Published - 5 Dec 2002

Bibliographical note

Funding Information:
We thank Dr Dong-Sup Lee for his helpful discussions and our laboratory members for their helpful inspiration to this study. J-H Kim and J-H Woo are elective students for this project (2001). This work was supported by Nuclear Research Funds from KISTEP to W-Y Park (1999 – 2001). This study was supported in part by 2001 BK21 project for Medicine, Dentistry and Pharmacy to M-J Kang, C-N Im, C-I Hwang, W-Y Park and J-S Seo.

Keywords

γ-irradiation
CDNA microarray
Cytoplasmic epoxide hydrolase
P53
Phospholipase Cγ2

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title = "Identification of radiation-specific responses from gene expression profile",

abstract = "The responses to ionizing radiation (IR) in tumors are dependent on cellular context. We investigated radiation-related expression patterns in Jurkat T cells with nonsense mutation in p53 using cDNA microarray. Expression of 2400 genes in γ-irradiated cells was distinct from other stimulations like anti-CD3, phetohemagglutinin (PHA) and concanavalin A (ConA) in unsupervised clustering analysis. Among them, 384 genes were selected for their IR-specific changes to make 'RadChip'. In spite of p53 status, every type of cells showed similar patterns in expression of these genes upon γ-radiation. Moreover, radiation-induced responses were clearly separated from the responses to other genotoxic stress like UV radiation, cisplatin and doxorubicin. We focused on two IR-related genes, phospholipase Cγ2 (PLCG2) and cytosolic epoxide hydrolase (EPHX2), which were increased at 12 h after γ-radiation in RT-PCR. TPCK could suppress the induction of these two genes in either of Jurkat T cells and PBMCs, which might suggest the transcriptional regulation of PLCG2 and EPHX2 by NF-κB upon γ-radiation. From these results, we could identify the IR-specific genes from expression profiling, which can be used as radiation biomarkers to screen radiation exposure as well as probing the mechanism of cellular responses to ionizing radiation.",

keywords = "γ-irradiation, CDNA microarray, Cytoplasmic epoxide hydrolase, P53, Phospholipase Cγ2",

author = "Park, {Woong Yang} and Hwang, {Chang Il} and Im, {Chang Nim} and Kang, {Min Ji} and Woo, {Jang Hee} and Kim, {Ju Hoon} and Kim, {Yon Su} and Kim, {Ju Han} and Ho Kim and Kim, {Kyung A.} and Yu, {Hyung Jin} and Lee, {Sue Jae} and Lee, {Yun Sil} and Seo, {Jeong Sun}",

note = "Funding Information: We thank Dr Dong-Sup Lee for his helpful discussions and our laboratory members for their helpful inspiration to this study. J-H Kim and J-H Woo are elective students for this project (2001). This work was supported by Nuclear Research Funds from KISTEP to W-Y Park (1999 – 2001). This study was supported in part by 2001 BK21 project for Medicine, Dentistry and Pharmacy to M-J Kang, C-N Im, C-I Hwang, W-Y Park and J-S Seo.",

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doi = "10.1038/sj.onc.1205977",

language = "English",

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AU - Park, Woong Yang

AU - Hwang, Chang Il

AU - Im, Chang Nim

AU - Kang, Min Ji

AU - Woo, Jang Hee

AU - Kim, Ju Hoon

AU - Kim, Yon Su

AU - Kim, Ju Han

AU - Kim, Ho

AU - Kim, Kyung A.

AU - Yu, Hyung Jin

AU - Lee, Sue Jae

AU - Lee, Yun Sil

AU - Seo, Jeong Sun

N1 - Funding Information: We thank Dr Dong-Sup Lee for his helpful discussions and our laboratory members for their helpful inspiration to this study. J-H Kim and J-H Woo are elective students for this project (2001). This work was supported by Nuclear Research Funds from KISTEP to W-Y Park (1999 – 2001). This study was supported in part by 2001 BK21 project for Medicine, Dentistry and Pharmacy to M-J Kang, C-N Im, C-I Hwang, W-Y Park and J-S Seo.

PY - 2002/12/5

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N2 - The responses to ionizing radiation (IR) in tumors are dependent on cellular context. We investigated radiation-related expression patterns in Jurkat T cells with nonsense mutation in p53 using cDNA microarray. Expression of 2400 genes in γ-irradiated cells was distinct from other stimulations like anti-CD3, phetohemagglutinin (PHA) and concanavalin A (ConA) in unsupervised clustering analysis. Among them, 384 genes were selected for their IR-specific changes to make 'RadChip'. In spite of p53 status, every type of cells showed similar patterns in expression of these genes upon γ-radiation. Moreover, radiation-induced responses were clearly separated from the responses to other genotoxic stress like UV radiation, cisplatin and doxorubicin. We focused on two IR-related genes, phospholipase Cγ2 (PLCG2) and cytosolic epoxide hydrolase (EPHX2), which were increased at 12 h after γ-radiation in RT-PCR. TPCK could suppress the induction of these two genes in either of Jurkat T cells and PBMCs, which might suggest the transcriptional regulation of PLCG2 and EPHX2 by NF-κB upon γ-radiation. From these results, we could identify the IR-specific genes from expression profiling, which can be used as radiation biomarkers to screen radiation exposure as well as probing the mechanism of cellular responses to ionizing radiation.

AB - The responses to ionizing radiation (IR) in tumors are dependent on cellular context. We investigated radiation-related expression patterns in Jurkat T cells with nonsense mutation in p53 using cDNA microarray. Expression of 2400 genes in γ-irradiated cells was distinct from other stimulations like anti-CD3, phetohemagglutinin (PHA) and concanavalin A (ConA) in unsupervised clustering analysis. Among them, 384 genes were selected for their IR-specific changes to make 'RadChip'. In spite of p53 status, every type of cells showed similar patterns in expression of these genes upon γ-radiation. Moreover, radiation-induced responses were clearly separated from the responses to other genotoxic stress like UV radiation, cisplatin and doxorubicin. We focused on two IR-related genes, phospholipase Cγ2 (PLCG2) and cytosolic epoxide hydrolase (EPHX2), which were increased at 12 h after γ-radiation in RT-PCR. TPCK could suppress the induction of these two genes in either of Jurkat T cells and PBMCs, which might suggest the transcriptional regulation of PLCG2 and EPHX2 by NF-κB upon γ-radiation. From these results, we could identify the IR-specific genes from expression profiling, which can be used as radiation biomarkers to screen radiation exposure as well as probing the mechanism of cellular responses to ionizing radiation.

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KW - CDNA microarray

KW - Cytoplasmic epoxide hydrolase

KW - P53

KW - Phospholipase Cγ2

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DO - 10.1038/sj.onc.1205977

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SN - 0950-9232

VL - 21

SP - 8521

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JO - Oncogene

JF - Oncogene

IS - 55

ER -

Identification of radiation-specific responses from gene expression profile

Abstract

Bibliographical note

Keywords

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