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Small GTPases - Ras and Rho01:24

Small GTPases - Ras and Rho

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Ras and Rho are small monomeric GTPases that act downstream of receptor tyrosine kinase (RTK) and regulate various cellular processes. These GTPases switch between active and inactive states by binding to guanine nucleotides.
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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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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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Cell polarity is the asymmetric distribution of cellular and membrane components, making one side of the cell different from the other. This polarity is essential to many processes such as embryogenesis, axon migration, glucose transport across epithelial cells, and directional cell migration. A migrating cell responds to intracellular or extracellular signals via molecular cascades that reorganize the actin cytoskeleton to establish this polarity. In these cells, the Rho family proteins Cdc42,...
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GTPases and their Regulation02:14

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Mapping Three Decades of Rho GTPase Signalling in Cancer: Unveiling Loopholes and Future Directions (1990-2024).

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Cell Biochemistry and Function
|January 16, 2026
PubMed
Summary

Rho GTPase signaling is crucial in cancer, but research is fragmented. This study highlights key areas like cell migration and breast cancer, while identifying gaps in atypical Rho GTPases and clinical translation for future cancer therapy research.

Keywords:
Cancer OncologyRho GTPasesVOSviewerbibliometric analysis

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Area of Science:

  • Oncology
  • Cell Biology
  • Bioinformatics

Background:

  • Rho GTPases regulate fundamental cell processes like migration and survival, and their dysregulation drives cancer.
  • Decades of research link Rho GTPase signaling to cancer, yet findings are dispersed across various contexts.
  • A comprehensive overview is needed to identify research trends and gaps in this field.

Purpose of the Study:

  • To conduct a bibliometric analysis of Rho GTPase research in cancer from 1990-2024.
  • To map the evolution of research focus, key players, and influential publications.
  • To identify current gaps and future directions for Rho GTPase-driven cancer research and therapy.

Main Methods:

  • Bibliometric analysis of 1,457 articles from Web of Science Core Collection (1990-2024).
  • Quantitative analysis using Microsoft Excel.
  • Visualization of collaboration, co-citation, and keyword networks using VOSviewer.

Main Results:

  • Publication rates surged after 2004, with 'Oncogene' as a leading journal and the US as the top contributing country.
  • Research predominantly focuses on epithelial-mesenchymal transition, invasion, metastasis, and breast cancer.
  • Canonical Rho GTPases (RhoA, Rac1, Cdc42) are heavily studied, while atypical Rho GTPases are underrepresented.
  • Clinical translation faces challenges due to signaling redundancy and tumor plasticity, not lack of research.

Conclusions:

  • Significant research exists on Rho GTPases in cancer, particularly canonical members and hallmarks like metastasis.
  • Gaps remain in understanding atypical Rho GTPases and integrating findings with immuno-oncology and precision medicine.
  • Future research should address these gaps to advance Rho GTPase-targeted cancer therapies.