Related Experiment Video

Updated: Aug 20, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

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Non-canonical Small GTPase RBJ Promotes NSCLC Progression Through the Canonical MEK/ERK Signaling Pathway

Yujin Wang1,2, Xiaoyan Shen3, Qingwen Wang1,2

  • 1Department of Thoracic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, China.

Current Pharmaceutical Design
|November 18, 2022
PubMed
Abstract

Insights

RBJ protein promotes non-small cell lung cancer (NSCLC) progression by activating epithelial-mesenchymal transition (EMT) via the MEK/ERK pathway. Targeting RBJ may offer a new therapeutic strategy for NSCLC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • The role of RBJ, a member of the small GTPase Ras superfamily, is largely unknown in non-small cell lung cancer (NSCLC).
  • Understanding RBJ's function is crucial for developing novel therapeutic strategies against NSCLC.

Purpose of the Study:

  • To elucidate the specific function of RBJ in the progression of non-small cell lung cancer (NSCLC).
  • To investigate the underlying molecular mechanisms by which RBJ influences NSCLC growth and metastasis.

Main Methods:

  • Immunohistochemistry (IHC) was used to quantify RBJ protein levels in NSCLC tumor and adjacent normal tissues.
  • In vitro assays (EdU, CCK8, colony formation, transwell, wound healing) assessed the impact of RBJ modulation on NSCLC cell proliferation, migration, and invasion.
  • A nude mouse xenograft model was employed to evaluate RBJ's role in tumorigenesis in vivo.

Main Results:

  • RBJ protein levels were significantly elevated in NSCLC tissues and correlated with advanced clinical stages.
  • RBJ knockdown inhibited NSCLC cell growth, migration, and invasion by suppressing epithelial-mesenchymal transition (EMT) through the MEK/ERK signaling pathway.
  • Conversely, RBJ overexpression enhanced tumor formation in vivo and promoted EMT.

Conclusions:

  • RBJ acts as an oncogene in NSCLC by promoting cancer progression through the activation of EMT via the MEK/ERK signaling pathway.
  • RBJ represents a potential therapeutic target for non-small cell lung cancer.
Keywords:
GTPaseMEK/ERKNSCLCRBJRas superfamilyepithelial-mesenchymal transition (EMT)

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