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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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Receptor Tyrosine Kinases

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Related Experiment Video

Updated: May 24, 2026

Method for the Isolation and Identification of mRNAs, microRNAs and Protein Components of Ribonucleoprotein Complexes from Cell Extracts using RIP-Chip

Method for the Isolation and Identification of mRNAs, microRNAs and Protein Components of Ribonucleoprotein Complexes from Cell Extracts using RIP-Chip

Published on: September 29, 2012

RhoB regulates uPAR signalling.

Daniela Alfano¹, Pia Ragno, M Patrizia Stoppelli

¹Randall Division of Cell and Molecular Biophysics, King's College London, New Hunt's House, Guy's Campus, London, UK.

Journal of Cell Science

|February 28, 2012

Summary

RhoB is crucial for cancer cell invasion and migration. Depleting RhoB significantly reduces prostate cancer cell invasion and migration by impacting urokinase plasminogen activator receptor (uPAR) signaling pathways.

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Method for the Isolation and Identification of mRNAs, microRNAs and Protein Components of Ribonucleoprotein Complexes from Cell Extracts using RIP-Chip

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Published on: June 21, 2016

Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

Urokinase-type plasminogen activator (uPA) and its receptor (uPAR) are vital in cancer cell adhesion, migration, and invasion.
Rho GTPases, particularly Rac1, are known regulators of uPA/uPAR-mediated cellular responses.

Purpose of the Study:

To investigate the role of Rho GTPases in uPA-stimulated prostate carcinoma cell migration and invasion.
To identify specific Rho GTPases involved in uPAR signaling pathways.

Main Methods:

RNA interference (RNAi) was used to deplete 12 different Rho GTPases.
Assays measured uPA-stimulated cell migration and invasion.
Western blotting and cell adhesion assays were performed to analyze protein expression, integrin levels, and signaling pathway activation.

Main Results:

Depletion of RhoB significantly reduced uPA-induced migration and invasion of prostate carcinoma cells.
RhoB depletion affected uPAR-induced integrin levels and inhibited signaling to cofilin, paxillin, and Akt.
uPAR activation of RhoB was observed, and RhoB depletion reduced cell adhesion and spreading on vitronectin.

Conclusions:

RhoB is a key regulator of uPAR signaling in prostate cancer cells.
RhoB plays a critical role in mediating uPAR-dependent cell adhesion, migration, and invasion.
Targeting RhoB may offer a therapeutic strategy for inhibiting cancer progression.