NDLI: Sequential inductions of the ZEB1 transcription factor caused by mutation of Rb and then Ras proteins are required for tumor initiation and progression.

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Sequential inductions of the ZEB1 transcription factor caused by mutation of Rb and then Ras proteins are required for tumor initiation and progression.

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Sequential inductions of the ZEB1 transcription factor caused by mutation of Rb and then Ras proteins are required for tumor initiation and progression.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Lu, Xiaoqin Jenson, Alfred B. Huang, Li Telang, Sucheta Cuatrecasas, Miriam Dean, Douglas C. Clem, Brian Liu, Yongqing Chesney, Jason Postigo, Antonio Sánchez-tilló, Ester
Description	Author Affiliation: Liu Y ( Molecular Targets Program, University of Louisville Health Sciences Center, Louisville, Kentucky 40202, USA.)
Abstract	Rb1 restricts cell cycle progression, and it imposes cell contact inhibition to suppress tumor outgrowth. It also triggers oncogene-induced senescence to block Ras mutation. Loss of the Rb1 pathway, which is a hallmark of cancer cells, then provides a permissive environment for Ras mutation, and Ras is sufficient for invasive tumor formation in Rb1 family mutant mouse embryo fibroblasts (MEFs). These results demonstrate that sequential mutation of the Rb1 and Ras pathways comprises a tumor initiation axis. Both Rb1 and Ras regulate expression of the transcription factor ZEB1, thereby linking tumor initiation to the subsequent invasion and metastasis, which is induced by ZEB1. ZEB1 acts in a negative feedback loop to block expression of miR-200, which is thought to facilitate tumor invasion and metastasis. However, ZEB1 also represses cyclin-dependent kinase (cdk) inhibitors to control the cell cycle; its mutation in MEFs leads to induction of these inhibitors and premature senescence. Here, we provide evidence for two sequential inductions of ZEB1 during Ras transformation of MEFs. Rb1 constitutively represses cdk inhibitors, and induction of ZEB1 when the Rb1 pathway is lost is required to maintain this repression, allowing for the classic immortalization and loss of cell contact inhibition seen when the Rb1 pathway is lost. In vivo, we show that this induction of ZEB1 is required for Ras-initiated tumor formation. ZEB1 is then further induced by Ras, beyond the level seen with Rb1 mutation, and this Ras superinduction is required to reach a threshold of ZEB1 sufficient for repression of miR-200 and tumor invasion.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	16
Volume Number	288
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2013-04-19
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell Transformation, Neoplastic Metabolism Homeodomain Proteins Kruppel-Like Transcription Factors Mutation Neoplasms Retinoblastoma Protein Ras Proteins Animals Cell Aging Genetics Pathology Embryo, Mammalian Fibroblasts Gene Expression Regulation, Neoplastic Mice Mice, Inbred BALB C Mice, Knockout Mice, Nude MicroRNAs Biosynthesis Neoplasm Invasiveness Neoplasm Metastasis RNA, Neoplasm Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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