Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition

Yeun Jin Ju; Hyun Jin Shin; Jeong Eun Park; Kyoung Mi Juhn; Seon Rang Woo; Hee Young Kim; Young Hoon Han; Sang Gu Hwang; Sung Hee Hong; Chang Mo Kang; Young Do Yoo; Won Bong Park; Myung Haing Cho; Gil Hong Park; Kee Ho Lee

doi:10.1016/j.bbrc.2010.09.091

Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition

Yeun Jin Ju, Hyun Jin Shin, Jeong Eun Park, Kyoung Mi Juhn, Seon Rang Woo, Hee Young Kim, Young Hoon Han, Sang Gu Hwang, Sung Hee Hong, Chang Mo Kang, Young Do Yoo, Won Bong Park, Myung Haing Cho, Gil Hong Park, Kee Ho Lee

Department of Biomedical Sciences

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

2 Citations (Scopus)

Abstract

A combination of a radiotherapeutic regimen with telomerase inhibition is valuable when tumor cells are to be sensitized to radiation. Here, we describe cell clones unresponsive to radiosensitization after telomere shortening. After extensive division of individual transformed clones of mTERC^-/- cells, about 22% of clones were unresponsive to radiosensitization even though telomerase action was inhibited. The telomere lengths of unsensitized mTERC^-/- clones were reduced, as were those of most sensitized clones. However, the unsensitized clones did not exhibit chromosomal end-to-end fusion to the extent noted in all sensitized clones. Thus, a defense mechanism preventing telomere erosion is operative even when telomeres become shorter under conditions of telomerase deficiency, and results in unresponsiveness to the radiosensitization generally mediated by telomere shortening.

Original language	English
Pages (from-to)	198-202
Number of pages	5
Journal	Biochemical and biophysical research communications
Volume	402
Issue number	2
DOIs	https://doi.org/10.1016/j.bbrc.2010.09.091
Publication status	Published - 2010 Nov 12

Bibliographical note

Funding Information:
This work was supported by a grant from the National Nuclear R & D program and BAERI, the Korean Ministry of Science and Technology . M.H.C. was supported by a grant from the Korea Research Foundation , funded by the Korean Government (Grant No. KRF-2006-311-E00507 ).

Keywords

Chromosomal end-to-end fusion
Radiosensitization
Telomere
Telomere length

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

Access to Document

10.1016/j.bbrc.2010.09.091

Cite this

Ju, Y. J., Shin, H. J., Park, J. E., Juhn, K. M., Woo, S. R., Kim, H. Y., Han, Y. H., Hwang, S. G., Hong, S. H., Kang, C. M., Yoo, Y. D., Park, W. B., Cho, M. H., Park, G. H., & Lee, K. H. (2010). Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition. Biochemical and biophysical research communications, 402(2), 198-202. https://doi.org/10.1016/j.bbrc.2010.09.091

@article{ac0a2e3566774e63b92925fb393b301a,

title = "Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition",

abstract = "A combination of a radiotherapeutic regimen with telomerase inhibition is valuable when tumor cells are to be sensitized to radiation. Here, we describe cell clones unresponsive to radiosensitization after telomere shortening. After extensive division of individual transformed clones of mTERC-/- cells, about 22% of clones were unresponsive to radiosensitization even though telomerase action was inhibited. The telomere lengths of unsensitized mTERC-/- clones were reduced, as were those of most sensitized clones. However, the unsensitized clones did not exhibit chromosomal end-to-end fusion to the extent noted in all sensitized clones. Thus, a defense mechanism preventing telomere erosion is operative even when telomeres become shorter under conditions of telomerase deficiency, and results in unresponsiveness to the radiosensitization generally mediated by telomere shortening.",

keywords = "Chromosomal end-to-end fusion, Radiosensitization, Telomere, Telomere length",

author = "Ju, {Yeun Jin} and Shin, {Hyun Jin} and Park, {Jeong Eun} and Juhn, {Kyoung Mi} and Woo, {Seon Rang} and Kim, {Hee Young} and Han, {Young Hoon} and Hwang, {Sang Gu} and Hong, {Sung Hee} and Kang, {Chang Mo} and Yoo, {Young Do} and Park, {Won Bong} and Cho, {Myung Haing} and Park, {Gil Hong} and Lee, {Kee Ho}",

note = "Funding Information: This work was supported by a grant from the National Nuclear R & D program and BAERI, the Korean Ministry of Science and Technology . M.H.C. was supported by a grant from the Korea Research Foundation , funded by the Korean Government (Grant No. KRF-2006-311-E00507 ).",

year = "2010",

month = nov,

day = "12",

doi = "10.1016/j.bbrc.2010.09.091",

language = "English",

volume = "402",

pages = "198--202",

journal = "Biochemical and biophysical research communications",

issn = "0006-291X",

publisher = "Academic Press Inc.",

number = "2",

}

TY - JOUR

T1 - Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition

AU - Ju, Yeun Jin

AU - Shin, Hyun Jin

AU - Park, Jeong Eun

AU - Juhn, Kyoung Mi

AU - Woo, Seon Rang

AU - Kim, Hee Young

AU - Han, Young Hoon

AU - Hwang, Sang Gu

AU - Hong, Sung Hee

AU - Kang, Chang Mo

AU - Yoo, Young Do

AU - Park, Won Bong

AU - Cho, Myung Haing

AU - Park, Gil Hong

AU - Lee, Kee Ho

N1 - Funding Information: This work was supported by a grant from the National Nuclear R & D program and BAERI, the Korean Ministry of Science and Technology . M.H.C. was supported by a grant from the Korea Research Foundation , funded by the Korean Government (Grant No. KRF-2006-311-E00507 ).

PY - 2010/11/12

Y1 - 2010/11/12

N2 - A combination of a radiotherapeutic regimen with telomerase inhibition is valuable when tumor cells are to be sensitized to radiation. Here, we describe cell clones unresponsive to radiosensitization after telomere shortening. After extensive division of individual transformed clones of mTERC-/- cells, about 22% of clones were unresponsive to radiosensitization even though telomerase action was inhibited. The telomere lengths of unsensitized mTERC-/- clones were reduced, as were those of most sensitized clones. However, the unsensitized clones did not exhibit chromosomal end-to-end fusion to the extent noted in all sensitized clones. Thus, a defense mechanism preventing telomere erosion is operative even when telomeres become shorter under conditions of telomerase deficiency, and results in unresponsiveness to the radiosensitization generally mediated by telomere shortening.

AB - A combination of a radiotherapeutic regimen with telomerase inhibition is valuable when tumor cells are to be sensitized to radiation. Here, we describe cell clones unresponsive to radiosensitization after telomere shortening. After extensive division of individual transformed clones of mTERC-/- cells, about 22% of clones were unresponsive to radiosensitization even though telomerase action was inhibited. The telomere lengths of unsensitized mTERC-/- clones were reduced, as were those of most sensitized clones. However, the unsensitized clones did not exhibit chromosomal end-to-end fusion to the extent noted in all sensitized clones. Thus, a defense mechanism preventing telomere erosion is operative even when telomeres become shorter under conditions of telomerase deficiency, and results in unresponsiveness to the radiosensitization generally mediated by telomere shortening.

KW - Chromosomal end-to-end fusion

KW - Radiosensitization

KW - Telomere

KW - Telomere length

UR - http://www.scopus.com/inward/record.url?scp=78149470396&partnerID=8YFLogxK

U2 - 10.1016/j.bbrc.2010.09.091

DO - 10.1016/j.bbrc.2010.09.091

M3 - Article

C2 - 20875790

AN - SCOPUS:78149470396

SN - 0006-291X

VL - 402

SP - 198

EP - 202

JO - Biochemical and biophysical research communications

JF - Biochemical and biophysical research communications

IS - 2

ER -

Clonal cell populations unresponsive to radiosensitization induced by telomerase inhibition

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this