Hydroxyurea-induced global transcriptional suppression in mouse ES cells

Peng Cui; Qiang Lin; Chengqi Xin; Lu Han; Lili An; Yulan Wang; Zhishang Hu; Feng Ding; Lingfang Zhang; Songnian Hu; Haiying Hang; Jun Yu

doi:10.1093/carcin/bgq106

Hydroxyurea-induced global transcriptional suppression in mouse ES cells

Peng Cui, Qiang Lin, Chengqi Xin, Lu Han, Lili An, Yulan Wang, Zhishang Hu, Feng Ding, Lingfang Zhang, Songnian Hu^*, Haiying Hang, Jun Yu

^*Corresponding author for this work

Biological, Environmental Sciences and Engineering

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

11 Scopus citations

Abstract

Hydroxyurea (HU), as a therapeutic medicine, has been extensively used clinically. To further survey molecular mechanisms of HU treatment, we analyzed global transcriptomic alteration of mouse ES cells in response to the treatment using high-throughput sequencing. We show that the global transcriptional activity is significantly suppressed as cells are exposed to HU treatment and alters multiple key cellular pathways, including cell cycle, apoptosis and DNAs. HU treatment also alters alternative splicing mechanisms and suppresses non-coding RNA expression. Our result provides novel clues for the understanding of how cells respond to HU and further suggests that high-throughput sequencing technology provides a powerful tool to study mechanisms of clinical drugs at the cellular level. Published by Oxford University Press 2010.

Original language	English (US)
Pages (from-to)	1661-1668
Number of pages	8
Journal	Carcinogenesis
Volume	31
Issue number	9
DOIs	https://doi.org/10.1093/carcin/bgq106
State	Published - May 31 2010

ASJC Scopus subject areas

Cancer Research

UN SDGs

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

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10.1093/carcin/bgq106

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@article{07483e92429c4179b3bc7ef50321c366,

title = "Hydroxyurea-induced global transcriptional suppression in mouse ES cells",

abstract = "Hydroxyurea (HU), as a therapeutic medicine, has been extensively used clinically. To further survey molecular mechanisms of HU treatment, we analyzed global transcriptomic alteration of mouse ES cells in response to the treatment using high-throughput sequencing. We show that the global transcriptional activity is significantly suppressed as cells are exposed to HU treatment and alters multiple key cellular pathways, including cell cycle, apoptosis and DNAs. HU treatment also alters alternative splicing mechanisms and suppresses non-coding RNA expression. Our result provides novel clues for the understanding of how cells respond to HU and further suggests that high-throughput sequencing technology provides a powerful tool to study mechanisms of clinical drugs at the cellular level. Published by Oxford University Press 2010.",

author = "Peng Cui and Qiang Lin and Chengqi Xin and Lu Han and Lili An and Yulan Wang and Zhishang Hu and Feng Ding and Lingfang Zhang and Songnian Hu and Haiying Hang and Jun Yu",

note = "Funding Information: National Basic Research Program (973 Program) (2006CB910401, 2006CB910403 and 2006CB910404 to J.Y. and S.H.); National Protein Project of Ministry of Science and Technology (2006CB910902 to H.H.); Ministry of Science and Technology of the People{\textquoteright}s Republic of China; Knowledge Innovation Program of Chinese Academy of Sciences (KSCX2-YW-R63 and KJCX2-YW-L08 to H.H.); National Natural Science Foundation of China (30530180 to H.H.).",

year = "2010",

month = may,

day = "31",

doi = "10.1093/carcin/bgq106",

language = "English (US)",

volume = "31",

pages = "1661--1668",

journal = "Carcinogenesis",

issn = "0143-3334",

publisher = "Oxford University Press",

number = "9",

}

TY - JOUR

T1 - Hydroxyurea-induced global transcriptional suppression in mouse ES cells

AU - Cui, Peng

AU - Lin, Qiang

AU - Xin, Chengqi

AU - Han, Lu

AU - An, Lili

AU - Wang, Yulan

AU - Hu, Zhishang

AU - Ding, Feng

AU - Zhang, Lingfang

AU - Hu, Songnian

AU - Hang, Haiying

AU - Yu, Jun

N1 - Funding Information: National Basic Research Program (973 Program) (2006CB910401, 2006CB910403 and 2006CB910404 to J.Y. and S.H.); National Protein Project of Ministry of Science and Technology (2006CB910902 to H.H.); Ministry of Science and Technology of the People’s Republic of China; Knowledge Innovation Program of Chinese Academy of Sciences (KSCX2-YW-R63 and KJCX2-YW-L08 to H.H.); National Natural Science Foundation of China (30530180 to H.H.).

PY - 2010/5/31

Y1 - 2010/5/31

N2 - Hydroxyurea (HU), as a therapeutic medicine, has been extensively used clinically. To further survey molecular mechanisms of HU treatment, we analyzed global transcriptomic alteration of mouse ES cells in response to the treatment using high-throughput sequencing. We show that the global transcriptional activity is significantly suppressed as cells are exposed to HU treatment and alters multiple key cellular pathways, including cell cycle, apoptosis and DNAs. HU treatment also alters alternative splicing mechanisms and suppresses non-coding RNA expression. Our result provides novel clues for the understanding of how cells respond to HU and further suggests that high-throughput sequencing technology provides a powerful tool to study mechanisms of clinical drugs at the cellular level. Published by Oxford University Press 2010.

AB - Hydroxyurea (HU), as a therapeutic medicine, has been extensively used clinically. To further survey molecular mechanisms of HU treatment, we analyzed global transcriptomic alteration of mouse ES cells in response to the treatment using high-throughput sequencing. We show that the global transcriptional activity is significantly suppressed as cells are exposed to HU treatment and alters multiple key cellular pathways, including cell cycle, apoptosis and DNAs. HU treatment also alters alternative splicing mechanisms and suppresses non-coding RNA expression. Our result provides novel clues for the understanding of how cells respond to HU and further suggests that high-throughput sequencing technology provides a powerful tool to study mechanisms of clinical drugs at the cellular level. Published by Oxford University Press 2010.

UR - http://www.scopus.com/inward/record.url?scp=77956283059&partnerID=8YFLogxK

U2 - 10.1093/carcin/bgq106

DO - 10.1093/carcin/bgq106

M3 - Article

C2 - 20513671

AN - SCOPUS:77956283059

SN - 0143-3334

VL - 31

SP - 1661

EP - 1668

JO - Carcinogenesis

JF - Carcinogenesis

IS - 9

ER -

Hydroxyurea-induced global transcriptional suppression in mouse ES cells

Abstract

ASJC Scopus subject areas

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