RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

S. Josson; Y. Xu; F. Fang; S. K. Dhar; D. K. St Clair; W. H. St. Clair

doi:10.1038/sj.onc.1209186

RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

S. Josson
, Y. Xu
, F. Fang
, S. K. Dhar
, D. K. St Clair
, W. H. St. Clair

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

86 Scopus citations

Abstract

The relationship between NF-κB and resistance to radiation treatment in many tumor cell types has been generally well recognized. However, which members of the NF-κB family contribute to radiation resistance is unclear. In the present study, we demonstrate that RelB plays an important radioprotective role in aggressive prostate cancer cells, in part by the induction of antioxidant and antiapoptotic manganese superoxide dismutase (MnSOD) gene. RelB is both constitutively present and is inducible by radiation in aggressive prostate cancer cells. Using ectopically expressed dominant negative inhibitor, p100 mutant, and the siRNA approach, we demonstrate that selective inhibition of RelB significantly decreases the levels of MnSOD resulting in a significant increase in the sensitivity of prostate cancer cells to radiation treatment. These results demonstrate that RelB plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death. Thus, inhibition of RelB could be a novel mechanism to radiosensitize prostate cancer.

Original language	English
Pages (from-to)	1554-1559
Number of pages	6
Journal	Oncogene
Volume	25
Issue number	10
DOIs	https://doi.org/10.1038/sj.onc.1209186
State	Published - Mar 9 2006

Bibliographical note

Funding Information:
We thank Dr Shao-Cong Sun for the p100 mutant plasmid. We are grateful to Dr Ali Meigooni, Professor of Physics in the Department of Radiation Medicine, for the dosimetry and calibration of the X-ray machine. This work was supported by the University of Kentucky Research Foundation and NIH grant CA 49797.

Funding

We thank Dr Shao-Cong Sun for the p100 mutant plasmid. We are grateful to Dr Ali Meigooni, Professor of Physics in the Department of Radiation Medicine, for the dosimetry and calibration of the X-ray machine. This work was supported by the University of Kentucky Research Foundation and NIH grant CA 49797.

Funders	Funder number
National Institutes of Health (NIH)
National Childhood Cancer Registry – National Cancer Institute	R01CA049797
National Childhood Cancer Registry – National Cancer Institute
Northern Kentucky University Research Foundation

UN SDGs

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

SDG 3 Good Health and Well-being

Keywords

MnSOD
Radiation
RelB

ASJC Scopus subject areas

Molecular Biology
Genetics
Cancer Research

Access to Document

10.1038/sj.onc.1209186

Cite this

@article{05a5415a821d46fcb5973afc0065ce47,

title = "RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells",

abstract = "The relationship between NF-κB and resistance to radiation treatment in many tumor cell types has been generally well recognized. However, which members of the NF-κB family contribute to radiation resistance is unclear. In the present study, we demonstrate that RelB plays an important radioprotective role in aggressive prostate cancer cells, in part by the induction of antioxidant and antiapoptotic manganese superoxide dismutase (MnSOD) gene. RelB is both constitutively present and is inducible by radiation in aggressive prostate cancer cells. Using ectopically expressed dominant negative inhibitor, p100 mutant, and the siRNA approach, we demonstrate that selective inhibition of RelB significantly decreases the levels of MnSOD resulting in a significant increase in the sensitivity of prostate cancer cells to radiation treatment. These results demonstrate that RelB plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death. Thus, inhibition of RelB could be a novel mechanism to radiosensitize prostate cancer.",

keywords = "MnSOD, Radiation, RelB",

author = "S. Josson and Y. Xu and F. Fang and Dhar, \{S. K.\} and \{St Clair\}, \{D. K.\} and \{St. Clair\}, \{W. H.\}",

note = "Funding Information: We thank Dr Shao-Cong Sun for the p100 mutant plasmid. We are grateful to Dr Ali Meigooni, Professor of Physics in the Department of Radiation Medicine, for the dosimetry and calibration of the X-ray machine. This work was supported by the University of Kentucky Research Foundation and NIH grant CA 49797.",

year = "2006",

month = mar,

day = "9",

doi = "10.1038/sj.onc.1209186",

language = "English",

volume = "25",

pages = "1554--1559",

number = "10",

}

TY - JOUR

T1 - RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

AU - Josson, S.

AU - Xu, Y.

AU - Fang, F.

AU - Dhar, S. K.

AU - St Clair, D. K.

AU - St. Clair, W. H.

N1 - Funding Information: We thank Dr Shao-Cong Sun for the p100 mutant plasmid. We are grateful to Dr Ali Meigooni, Professor of Physics in the Department of Radiation Medicine, for the dosimetry and calibration of the X-ray machine. This work was supported by the University of Kentucky Research Foundation and NIH grant CA 49797.

PY - 2006/3/9

Y1 - 2006/3/9

N2 - The relationship between NF-κB and resistance to radiation treatment in many tumor cell types has been generally well recognized. However, which members of the NF-κB family contribute to radiation resistance is unclear. In the present study, we demonstrate that RelB plays an important radioprotective role in aggressive prostate cancer cells, in part by the induction of antioxidant and antiapoptotic manganese superoxide dismutase (MnSOD) gene. RelB is both constitutively present and is inducible by radiation in aggressive prostate cancer cells. Using ectopically expressed dominant negative inhibitor, p100 mutant, and the siRNA approach, we demonstrate that selective inhibition of RelB significantly decreases the levels of MnSOD resulting in a significant increase in the sensitivity of prostate cancer cells to radiation treatment. These results demonstrate that RelB plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death. Thus, inhibition of RelB could be a novel mechanism to radiosensitize prostate cancer.

AB - The relationship between NF-κB and resistance to radiation treatment in many tumor cell types has been generally well recognized. However, which members of the NF-κB family contribute to radiation resistance is unclear. In the present study, we demonstrate that RelB plays an important radioprotective role in aggressive prostate cancer cells, in part by the induction of antioxidant and antiapoptotic manganese superoxide dismutase (MnSOD) gene. RelB is both constitutively present and is inducible by radiation in aggressive prostate cancer cells. Using ectopically expressed dominant negative inhibitor, p100 mutant, and the siRNA approach, we demonstrate that selective inhibition of RelB significantly decreases the levels of MnSOD resulting in a significant increase in the sensitivity of prostate cancer cells to radiation treatment. These results demonstrate that RelB plays an important role in redox regulation of the cell and protects aggressive prostate cancer cells against radiation-induced cell death. Thus, inhibition of RelB could be a novel mechanism to radiosensitize prostate cancer.

KW - MnSOD

KW - Radiation

KW - RelB

UR - https://www.scopus.com/pages/publications/33644837287

UR - https://www.scopus.com/pages/publications/33644837287#tab=citedBy

U2 - 10.1038/sj.onc.1209186

DO - 10.1038/sj.onc.1209186

M3 - Article

C2 - 16261162

AN - SCOPUS:33644837287

SN - 0950-9232

VL - 25

SP - 1554

EP - 1559

JO - Oncogene

JF - Oncogene

IS - 10

ER -

RelB regulates manganese superoxide dismutase gene and resistance to ionizing radiation of prostate cancer cells

Abstract

Bibliographical note

Funding

UN SDGs

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this