Crept accelerates tumorigenesis by regulating the transcription of cell-cycle-related genes

Dongdong Lu; Yinyuan Wu; Yinyin Wang; Fangli Ren; Dianjun Wang; Fuqin Su; Yanquan Zhang; Xi Yang; Guihua Jin; Xinbao Hao; Dacheng He; Yonggong Zhai; David M. Irwin; Jim Hu; Joseph J.Y. Sung; Jun Yu; Baoqing Jia; Zhijie Chang

doi:10.1016/j.ccr.2011.12.016

Crept accelerates tumorigenesis by regulating the transcription of cell-cycle-related genes

Dongdong Lu, Yinyuan Wu, Yinyin Wang, Fangli Ren, Dianjun Wang, Fuqin Su, Yanquan Zhang, Xi Yang, Guihua Jin, Xinbao Hao, Dacheng He, Yonggong Zhai, David M. Irwin, Jim Hu, Joseph J.Y. Sung, Jun Yu, Baoqing Jia, Zhijie Chang

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

71 Scopus citations

Abstract

Tumorigenesis is caused by an uncontrolled cell cycle and the altered expression of many genes. Here, we report a gene CREPT that is preferentially expressed in diverse human tumors. Overexpression of CREPT accelerates tumor growth, whereas depletion of CREPT demonstrates a reversed effect. CREPT regulates cyclin D1 expression by binding to its promoter, enhancing its transcription both invivo and invitro, and interacting with RNA polymerase II (RNAPII). Interestingly, CREPT promotes the formation of a chromatin loop and prevents RNAPII from reading through the 3' end termination site of the gene. Our findings reveal a mechanism where CREPT increases cyclin D1 transcription during tumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.

Original language	English
Pages (from-to)	92-104
Number of pages	13
Journal	Cancer Cell
Volume	21
Issue number	1
DOIs	https://doi.org/10.1016/j.ccr.2011.12.016
State	Published - Jan 17 2012

Bibliographical note

Funding Information:
We thank Drs. Xiao-Fan Wang, Xin-Yuan Fu, and Robert Eisenman for their suggestions and discussions in this project. We thank Dr. Yang Shi for siRNA protocols and vectors. We thank Dr. Ya Gu in the Third People's Hospital of Qidong, Profs. Weibing Wang and Yaoyi Wu in Wuxi 101 Hospital in China for providing tumor samples, and Dr. Huijuan Zhang in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University for technical support. This work was supported by grants from the 973 Project (2006CB910102, 2011CB910502), the NSFC (31071225, 30228007, 30871286), the 863 project (2007AA021505), the MOST projects (2011ZX0811-006, 2009ZX08009, 2006CB910102) in China, a China-Canada Joint Health Research Initiative grant to J.H. (#CCI-82411) and Z.C. (#30611120522), and the Tsinghua Internal Foundation (20091081322).

Funding

We thank Drs. Xiao-Fan Wang, Xin-Yuan Fu, and Robert Eisenman for their suggestions and discussions in this project. We thank Dr. Yang Shi for siRNA protocols and vectors. We thank Dr. Ya Gu in the Third People's Hospital of Qidong, Profs. Weibing Wang and Yaoyi Wu in Wuxi 101 Hospital in China for providing tumor samples, and Dr. Huijuan Zhang in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University for technical support. This work was supported by grants from the 973 Project (2006CB910102, 2011CB910502), the NSFC (31071225, 30228007, 30871286), the 863 project (2007AA021505), the MOST projects (2011ZX0811-006, 2009ZX08009, 2006CB910102) in China, a China-Canada Joint Health Research Initiative grant to J.H. (#CCI-82411) and Z.C. (#30611120522), and the Tsinghua Internal Foundation (20091081322).

Funders	Funder number
863 project	2007AA021505
973 Project of Ministry of Science and Technology of China	2006CB910102, 2011CB910502
China-Canada Joint Health Research Initiative	-82411, 30611120522
Tsinghua Internal Foundation	20091081322
National Natural Science Foundation of China (NSFC)	30228007, 31071225, 30871286
National Natural Science Foundation of China (NSFC)
Ministry of Science and Technology	2011ZX0811-006, 2009ZX08009
Ministry of Science and Technology

ASJC Scopus subject areas

Oncology
Cancer Research

UN SDGs

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

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10.1016/j.ccr.2011.12.016

Cite this

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title = "Crept accelerates tumorigenesis by regulating the transcription of cell-cycle-related genes",

abstract = "Tumorigenesis is caused by an uncontrolled cell cycle and the altered expression of many genes. Here, we report a gene CREPT that is preferentially expressed in diverse human tumors. Overexpression of CREPT accelerates tumor growth, whereas depletion of CREPT demonstrates a reversed effect. CREPT regulates cyclin D1 expression by binding to its promoter, enhancing its transcription both invivo and invitro, and interacting with RNA polymerase II (RNAPII). Interestingly, CREPT promotes the formation of a chromatin loop and prevents RNAPII from reading through the 3' end termination site of the gene. Our findings reveal a mechanism where CREPT increases cyclin D1 transcription during tumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.",

author = "Dongdong Lu and Yinyuan Wu and Yinyin Wang and Fangli Ren and Dianjun Wang and Fuqin Su and Yanquan Zhang and Xi Yang and Guihua Jin and Xinbao Hao and Dacheng He and Yonggong Zhai and Irwin, {David M.} and Jim Hu and Sung, {Joseph J.Y.} and Jun Yu and Baoqing Jia and Zhijie Chang",

note = "Funding Information: We thank Drs. Xiao-Fan Wang, Xin-Yuan Fu, and Robert Eisenman for their suggestions and discussions in this project. We thank Dr. Yang Shi for siRNA protocols and vectors. We thank Dr. Ya Gu in the Third People's Hospital of Qidong, Profs. Weibing Wang and Yaoyi Wu in Wuxi 101 Hospital in China for providing tumor samples, and Dr. Huijuan Zhang in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University for technical support. This work was supported by grants from the 973 Project (2006CB910102, 2011CB910502), the NSFC (31071225, 30228007, 30871286), the 863 project (2007AA021505), the MOST projects (2011ZX0811-006, 2009ZX08009, 2006CB910102) in China, a China-Canada Joint Health Research Initiative grant to J.H. (#CCI-82411) and Z.C. (#30611120522), and the Tsinghua Internal Foundation (20091081322). ",

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AU - Lu, Dongdong

AU - Wu, Yinyuan

AU - Wang, Yinyin

AU - Ren, Fangli

AU - Wang, Dianjun

AU - Su, Fuqin

AU - Zhang, Yanquan

AU - Yang, Xi

AU - Jin, Guihua

AU - Hao, Xinbao

AU - He, Dacheng

AU - Zhai, Yonggong

AU - Irwin, David M.

AU - Hu, Jim

AU - Sung, Joseph J.Y.

AU - Yu, Jun

AU - Jia, Baoqing

AU - Chang, Zhijie

N1 - Funding Information: We thank Drs. Xiao-Fan Wang, Xin-Yuan Fu, and Robert Eisenman for their suggestions and discussions in this project. We thank Dr. Yang Shi for siRNA protocols and vectors. We thank Dr. Ya Gu in the Third People's Hospital of Qidong, Profs. Weibing Wang and Yaoyi Wu in Wuxi 101 Hospital in China for providing tumor samples, and Dr. Huijuan Zhang in the International Peace Maternity and Child Health Hospital, Shanghai Jiao Tong University for technical support. This work was supported by grants from the 973 Project (2006CB910102, 2011CB910502), the NSFC (31071225, 30228007, 30871286), the 863 project (2007AA021505), the MOST projects (2011ZX0811-006, 2009ZX08009, 2006CB910102) in China, a China-Canada Joint Health Research Initiative grant to J.H. (#CCI-82411) and Z.C. (#30611120522), and the Tsinghua Internal Foundation (20091081322).

PY - 2012/1/17

Y1 - 2012/1/17

N2 - Tumorigenesis is caused by an uncontrolled cell cycle and the altered expression of many genes. Here, we report a gene CREPT that is preferentially expressed in diverse human tumors. Overexpression of CREPT accelerates tumor growth, whereas depletion of CREPT demonstrates a reversed effect. CREPT regulates cyclin D1 expression by binding to its promoter, enhancing its transcription both invivo and invitro, and interacting with RNA polymerase II (RNAPII). Interestingly, CREPT promotes the formation of a chromatin loop and prevents RNAPII from reading through the 3' end termination site of the gene. Our findings reveal a mechanism where CREPT increases cyclin D1 transcription during tumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.

AB - Tumorigenesis is caused by an uncontrolled cell cycle and the altered expression of many genes. Here, we report a gene CREPT that is preferentially expressed in diverse human tumors. Overexpression of CREPT accelerates tumor growth, whereas depletion of CREPT demonstrates a reversed effect. CREPT regulates cyclin D1 expression by binding to its promoter, enhancing its transcription both invivo and invitro, and interacting with RNA polymerase II (RNAPII). Interestingly, CREPT promotes the formation of a chromatin loop and prevents RNAPII from reading through the 3' end termination site of the gene. Our findings reveal a mechanism where CREPT increases cyclin D1 transcription during tumorigenesis, through enhancing the recruitment of RNAPII to the promoter region, possibly, as well as chromatin looping.

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Crept accelerates tumorigenesis by regulating the transcription of cell-cycle-related genes

Abstract

Bibliographical note

Funding

ASJC Scopus subject areas

UN SDGs

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