Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase

Xuanmao Jiao; Sanjay Katiyar; Manran Liu; Susette C. Mueller; Michael P. Lisanti; Anping Li; Timothy G. Pestell; Kongming Wu; Xiaoming Ju; Zhiping Li; Erwin F. Wagner; Tatsuo Takeya; Chenguang Wang; Richard G. Pestell

doi:10.1091/mbc.E07-08-0753

Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase

Xuanmao Jiao, Sanjay Katiyar, Manran Liu, Susette C. Mueller, Michael P. Lisanti, Anping Li, Timothy G. Pestell, Kongming Wu, Xiaoming Ju, Zhiping Li, Erwin F. Wagner, Tatsuo Takeya, Chenguang Wang, Richard G. Pestell

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

Abstract

The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the activator protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-junf/f) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration, and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun-/- cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun-/- cells. As c-Src is a critical component of pathways regulating proliferation, survival, and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion. © 2008 by The American Society for Cell Biology.

Original language	English
Pages (from-to)	1378-1390
Number of pages	12
Journal	Molecular Biology of the Cell
Volume	19
Issue number	4
DOIs	https://doi.org/10.1091/mbc.E07-08-0753
Publication status	Published - Apr 2008

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10.1091/mbc.E07-08-0753

http://www.molbiolcell.org/cgi/reprint/19/4/1378

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Jiao, X., Katiyar, S., Liu, M., Mueller, S. C., Lisanti, M. P., Li, A., Pestell, T. G., Wu, K., Ju, X., Li, Z., Wagner, E. F., Takeya, T., Wang, C., & Pestell, R. G. (2008). Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase. Molecular Biology of the Cell, 19(4), 1378-1390. https://doi.org/10.1091/mbc.E07-08-0753

@article{bd2bd0b9d50642168d007277d51e4871,

title = "Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase",

abstract = "The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the activator protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-junf/f) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration, and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun-/- cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun-/- cells. As c-Src is a critical component of pathways regulating proliferation, survival, and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion. {\textcopyright} 2008 by The American Society for Cell Biology.",

author = "Xuanmao Jiao and Sanjay Katiyar and Manran Liu and Mueller, {Susette C.} and Lisanti, {Michael P.} and Anping Li and Pestell, {Timothy G.} and Kongming Wu and Xiaoming Ju and Zhiping Li and Wagner, {Erwin F.} and Tatsuo Takeya and Chenguang Wang and Pestell, {Richard G.}",

note = "CA51008-13, NCI NIH HHS, United StatesP30CA56036, NCI NIH HHS, United StatesR01CA70896, NCI NIH HHS, United StatesR01CA75503, NCI NIH HHS, United StatesR01CA86072, NCI NIH HHS, United States",

year = "2008",

month = apr,

doi = "10.1091/mbc.E07-08-0753",

language = "English",

volume = "19",

pages = "1378--1390",

journal = "Molecular Biology of the Cell",

issn = "1059-1524",

publisher = "American Society for Cell Biology",

number = "4",

}

Jiao, X, Katiyar, S, Liu, M, Mueller, SC, Lisanti, MP, Li, A, Pestell, TG, Wu, K, Ju, X, Li, Z, Wagner, EF, Takeya, T, Wang, C & Pestell, RG 2008, 'Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase', Molecular Biology of the Cell, vol. 19, no. 4, pp. 1378-1390. https://doi.org/10.1091/mbc.E07-08-0753

TY - JOUR

T1 - Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase

AU - Jiao, Xuanmao

AU - Katiyar, Sanjay

AU - Liu, Manran

AU - Mueller, Susette C.

AU - Lisanti, Michael P.

AU - Li, Anping

AU - Pestell, Timothy G.

AU - Wu, Kongming

AU - Ju, Xiaoming

AU - Li, Zhiping

AU - Wagner, Erwin F.

AU - Takeya, Tatsuo

AU - Wang, Chenguang

AU - Pestell, Richard G.

N1 - CA51008-13, NCI NIH HHS, United StatesP30CA56036, NCI NIH HHS, United StatesR01CA70896, NCI NIH HHS, United StatesR01CA75503, NCI NIH HHS, United StatesR01CA86072, NCI NIH HHS, United States

PY - 2008/4

Y1 - 2008/4

N2 - The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the activator protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-junf/f) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration, and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun-/- cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun-/- cells. As c-Src is a critical component of pathways regulating proliferation, survival, and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion. © 2008 by The American Society for Cell Biology.

AB - The spread of metastatic tumors to different organs is associated with poor prognosis. The metastatic process requires migration and cellular invasion. The protooncogene c-jun encodes the founding member of the activator protein-1 family and is required for cellular proliferation and DNA synthesis in response to oncogenic signals and plays an essential role in chemical carcinogenesis. The role of c-Jun in cellular invasion remains to be defined. Genetic deletion of c-Jun in transgenic mice is embryonic lethal; therefore, transgenic mice encoding a c-Jun gene flanked by LoxP sites (c-junf/f) were used. c-jun gene deletion reduced c-Src expression, hyperactivated ROCK II signaling, and reduced cellular polarity, migration, and invasiveness. c-Jun increased c-Src mRNA abundance and c-Src promoter activity involving an AP-1 site in the c-Src promoter. Transduction of c-jun-/- cells with either c-Jun or c-Src retroviral expression systems restored the defective cellular migration of c-jun-/- cells. As c-Src is a critical component of pathways regulating proliferation, survival, and metastasis, the induction of c-Src abundance, by c-Jun, provides a novel mechanism of cooperative signaling in cellular invasion. © 2008 by The American Society for Cell Biology.

U2 - 10.1091/mbc.E07-08-0753

DO - 10.1091/mbc.E07-08-0753

M3 - Article

C2 - 18216279

SN - 1059-1524

VL - 19

SP - 1378

EP - 1390

JO - Molecular Biology of the Cell

JF - Molecular Biology of the Cell

IS - 4

ER -

Disruption of c-Jun reduces cellular migration and invasion through inhibition of c-Src and hyperactivation of ROCK II kinase

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