Role of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair

被引：12

作者：

Tanikawa, M. ^{[1
]}

Wada-Hiraike, O. ^{[1
]}

Yoshizawa-Sugata, N. ^{[2
]}

Shirane, A. ^{[1
]}

Hirano, M. ^{[1
]}

Hiraike, H. ^{[1
]}

Miyamoto, Y. ^{[1
]}

Sone, K. ^{[1
]}

Ikeda, Y. ^{[1
]}

Kashiyama, T. ^{[1
]}

Oda, K. ^{[1
]}

Kawana, K. ^{[1
]}

Katakura, Y. ^{[3
]}

Yano, T. ^{[4
]}

Masai, H. ^{[2
]}

Roy, A. L. ^{[5
]}

Osuga, Y. ^{[1
]}

Fujii, T. ^{[1
]}

机构：

[1] Univ Tokyo, Grad Sch Med, Dept Obstet & Gynecol, Bunkyo Ku, Tokyo 1138655, Japan

[2] Tokyo Metropolitan Inst Med Sci, Genome Dynam Project, Setagaya Ku, Tokyo 1568506, Japan

[3] Kyushu Univ, Grad Sch Syst Life Sci, Higashi Ku, Fukuoka 8128581, Japan

[4] Natl Ctr Global Hlth & Med, Dept Obstet & Gynecol, Shinjyuku Ku, Tokyo 1628655, Japan

[5] Tufts Univ, Sch Med, Sackler Sch Biomed Sci, Dept Pathol, Boston, MA 02111 USA

来源：

BRITISH JOURNAL OF CANCER | 2013年 / 109卷 / 12期

关键词：

TFII-I; DBC1; cell cycle; DNA damage repair; homologous recombination; transcription factor; ESTROGEN-RECEPTOR-ALPHA; GENE-EXPRESSION; SIRT1; BRCA1; PROMOTER; DEACETYLASE; CHECKPOINT; INTERACTS; PROTEINS; CLONING;

D O I：

10.1038/bjc.2013.532

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Background: In multicellular organisms, precise control of cell cycle and the maintenance of genomic stability are crucial to prevent chromosomal alterations. The accurate function of the DNA damage pathway is maintained by DNA repair mechanisms including homologous recombination (HR). Herein, we show that both TFII-I and DBC1 mediate cellular mechanisms of cell-cycle regulation and DNA double strand damage repair. Methods: Regulation of cell cycle by TFII-I and DBC1 was investigated using Trypan blue dye exclusion test, luciferase assay, and flow cytometry analysis. We also analysed the role of TFII-I and DBC1 in DNA double strand damage repair after irradiation by immunofluorescence study, clonogenicity assay, and HR assay. Results: Flow cytometry analysis revealed a novel function that siRNA-mediated knockdown of endogenous DBC1 resulted in G2/M phase arrest. We also have shown that both endogenous TFII-I and DBC1 activate DNA repair mechanisms after irradiation because irradiation-induced foci formation of TFII-I-gamma H2AX was observed, and the depletion of endogenous TFII-I or DBC1 resulted in the inhibition of normal HR efficiency. Conclusion: These results reveal novel mechanisms by which TFII-I and DBC1 can modulate cellular fate by affecting cell-cycle control as well as HR pathway.

引用

页码：3042 / 3048

页数：7

共 5 条

[1] Role of multifunctional transcription factor TFII-I and putative tumour suppressor DBC1 in cell cycle and DNA double strand damage repair
M Tanikawa
O Wada-Hiraike
N Yoshizawa-Sugata
A Shirane
M Hirano
H Hiraike
Y Miyamoto
K Sone
Y Ikeda
T Kashiyama
K Oda
K Kawana
Y Katakura
T Yano
H Masai
A L Roy
Y Osuga
T Fujii
British Journal of Cancer, 2013, 109 : 3042 - 3048
[2] Role of the multifunctional transcription factor TFII-I in DNA damage repair
Roy, Ananda L.
DNA REPAIR, 2021, 106
[3] The role of NBS1 in DNA double strand break repair, telomere stability, and cell cycle checkpoint control
Zhang, Y
Zhou, JQ
Lim, CUK
CELL RESEARCH, 2006, 16 (01) : 45 - 54
[4] The role of NBS1 in DNA double strand break repair, telomere stability, and cell cycle checkpoint control
Ying Zhang
Junqing Zhou
Chang UK Lim
Cell Research, 2006, 16 : 45 - 54
[5] Role of the casein kinase I isoform, Hrr25, and the cell cycle-regulatory transcription factor, SBF, in the transcriptional response to DNA damage in Saccharomyces cerevisiae
Ho, Y
Mason, S
Kobayashi, R
Hoekstra, M
Andrews, B
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (02) : 581 - 586

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