The Role of Rho GTPases in Cancer

A special issue of Cancers (ISSN 2072-6694).

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 3057

Special Issue Editors


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Guest Editor
1. Molecular Oncology Unit, Instituto de Inmunología Clínica y Experimental de Rosario (IDICER; CONICET-UNR), Centro de Investigación y Producción de Reactivos Biológicos (CIPReB; FCM-UNR), Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Santa Fe 3100 Rosario, Argentina
2. Mechanisms of Cancer Program, Centro de Investigación del Cáncer, CSIC-University of Salamanca, 37007 Salamanca, Spain
Interests: Rho GTPases; Vav proteins; synucleins; melanoma; drug repositioning; therapy resistance

E-Mail Website
Guest Editor
Molecular Mechanisms of Cancer Program, Centro de Investigación del Cáncer, CSIC-University of Salamanca, 37007 Salamanca, Spain
Interests: GTPases; RHO GEFs; oncogene; tumor suppressor; mutations; leukemias/lymphomas; mouse models

Special Issue Information

Dear Colleagues,

The Rho family of GTPases are key molecular switches that regulate actin cytoskeletal dynamics, coordinating a wide range of cellular processes including cell migration, intracellular signaling, and cell cycle progression. Dysregulation of Rho GTPases is seen in different types of cancer and is associated with cancer progression, development of metastases, and resistance to therapies. Targeting Rho GTPase signaling emerges as a therapeutic option for cancer therapy, particularly in combination with other anticancer agents.

We are pleased to invite you to participate in this Special Issue with a high-quality article or review (including basic, translational, and clinical studies on all tumor types), highlighting the role of Rho GTPases in cancer. The Rho family of GTPases is well known for their roles in regulating cell migration, and they also contribute to a variety of other cellular responses related to cancer and metastasis development and therapy resistance acquisition. This Special Issue aims to highlight the relevance of Rho GTPases in cellular pathways leading to cancer progression, metastasis development, and resistance acquisition.

In this Special Issue, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following:

  • Molecular signaling controlled by Rho GTPases in cancer;
  • Involvement of typical and atypical Rho GTPases in different types of cancers;
  • Molecular modulators of Rho GTPases in cancer;
  • Targeting Rho GTPasess for cancer treatment;
  • Rho GTPases and resistance to different cancer therapies;
  • Pharmacological inhibition of Rho GTPases-related pathways.

We look forward to receiving your contributions.

Dr. Mauricio A. Menacho-Márquez
Dr. Javier Robles-Valero
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Rho GTPases
  • GEFs
  • GAPs
  • GDIs
  • cancer
  • metastasis
  • chemotherapy resistance
  • immunotherapy
  • EMT
  • inhibitors

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Published Papers (1 paper)

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Research

14 pages, 2713 KiB  
Article
Preclinical Efficacy and Toxicology Evaluation of RAC1 Inhibitor 1A-116 in Human Glioblastoma Models
by Georgina A. Cardama, Julian Maggio, Lucas Valdez Capuccino, Nazareno Gonzalez, Valentina Matiller, Hugo H. Ortega, German R. Perez, Ignacio A. Demarco, Eduardo Spitzer, Daniel E. Gomez, Pablo Lorenzano Menna and Daniel F. Alonso
Cancers 2022, 14(19), 4810; https://doi.org/10.3390/cancers14194810 - 30 Sep 2022
Cited by 4 | Viewed by 2655
Abstract
Malignant gliomas are the most common primary central nervous system tumor in adults. Despite current therapeutics, these tumors are associated with poor prognosis and a median survival of 16 to 19 months. This highlights the need for innovative treatments for this incurable disease. [...] Read more.
Malignant gliomas are the most common primary central nervous system tumor in adults. Despite current therapeutics, these tumors are associated with poor prognosis and a median survival of 16 to 19 months. This highlights the need for innovative treatments for this incurable disease. Rac1 has long been associated with tumor progression and plays a key role in glioma’s infiltrative and invasive nature. The aim of this study is to evaluate the 1A-116 molecule, a Rac1 inhibitor, as targeted therapy for this aggressive disease. We found that targeting Rac1 inhibits cell proliferation and cell cycle progression using different in vitro human glioblastoma models. Additionally, we evaluated 1A-116 in vivo, showing a favorable toxicological profile. Using in silico tools, 1A-116 is also predicted to penetrate the blood–brain barrier and present a favorable metabolic fate. In line with these results, 1A-116 i.p daily treatment resulted in a dose-dependent antitumor effect in an orthotopic IDH-wt glioma model. Altogether, our study provides a strong potential for clinical translation of 1A-116 as a signal transduction-based precision therapy for glioma and also increases the evidence of Rac1 as a key molecular target. Full article
(This article belongs to the Special Issue The Role of Rho GTPases in Cancer)
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