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Updated: May 1, 2026

Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells
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Spatio-Temporal Manipulation of Small GTPase Activity at Subcellular Level and on Timescale of Seconds in Living Cells

Published on: March 9, 2012

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Small GTPase RBJ mediates nuclear entrapment of MEK1/MEK2 in tumor progression

Taoyong Chen1, Mingjin Yang1, Zhou Yu2

  • 1National Key Laboratory of Medical Immunology and Institute of Immunology, Second Military Medical University, Shanghai 200433, China; National Key Laboratory of Medical Molecular Biology and Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Beijing 100005, China.

Cancer Cell
|April 22, 2014
PubMed

Insights

RBJ, a Ras-related GTPase, drives gastrointestinal cancers by trapping MEK/ERK in the nucleus, promoting tumor growth. Its deficiency halts cancer progression, suggesting RBJ as an oncogenic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Ras-related small GTPases are crucial in cancer development.
  • The specific role of RBJ, a member of the sixth Ras GTPase subfamily, in tumorigenesis is largely unknown.

Purpose of the Study:

  • To investigate the role of RBJ in human gastrointestinal cancers.
  • To elucidate the mechanism by which RBJ influences carcinogenesis and tumor progression.

Main Methods:

  • Analysis of RBJ dysregulation in human gastrointestinal cancers.
  • Investigating RBJ's effect on nuclear localization of MEK1/MEK2 and ERK1/ERK2 activation.
  • Utilizing AOM/DSS-induced colonic carcinogenesis models in mice.
  • Assessing the impact of Rbj deficiency and knockdown on tumor development and growth.

Main Results:

  • RBJ is found to be dysregulated in human gastrointestinal cancers.
  • RBJ promotes carcinogenesis and tumor progression by causing nuclear entrapment of MEK1/MEK2.
  • Nucleus-localized RBJ prolongs the activation duration of the MEK/ERK pathway.
  • Rbj deficiency impairs AOM/DSS-induced colonic carcinogenesis and inhibits established tumor growth.

Conclusions:

  • RBJ acts as an oncogenic Ras-related small GTPase in gastrointestinal cancers.
  • RBJ facilitates tumor progression by mediating the nuclear accumulation of active MEK1/MEK2.
  • RBJ represents a potential therapeutic target for gastrointestinal malignancies.

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