The effects of mutant Ras proteins on the cell signalome.

Tamás Takács, Gyöngyi Kudlik, Anita Kurilla, Bálint Szeder, László Buday, Virag Vas
Author Information
  1. Tamás Takács: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
  2. Gyöngyi Kudlik: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
  3. Anita Kurilla: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
  4. Bálint Szeder: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
  5. László Buday: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary.
  6. Virag Vas: Institute of Enzymology, Research Centre for Natural Sciences, Budapest, Hungary. vas.virag@ttk.hu.

Abstract

The genetic alterations in cancer cells are tightly linked to signaling pathway dysregulation. Ras is a key molecule that controls several tumorigenesis-related processes, and mutations in RAS genes often lead to unbiased intensification of signaling networks that fuel cancer progression. In this article, we review recent studies that describe mutant Ras-regulated signaling routes and their cross-talk. In addition to the two main Ras-driven signaling pathways, i.e., the RAF/MEK/ERK and PI3K/AKT/mTOR pathways, we have also collected emerging data showing the importance of Ras in other signaling pathways, including the RAC/PAK, RalGDS/Ral, and PKC/PLC signaling pathways. Moreover, microRNA-regulated Ras-associated signaling pathways are also discussed to highlight the importance of Ras regulation in cancer. Finally, emerging data show that the signal alterations in specific cell types, such as cancer stem cells, could promote cancer development. Therefore, we also cover the up-to-date findings related to Ras-regulated signal transduction in cancer stem cells.

Keywords

References

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MeSH Term

Animals
Humans
Mutation
Neoplasms
Proto-Oncogene Proteins p21(ras)
Signal Transduction

Chemicals

Proto-Oncogene Proteins p21(ras)

Word Cloud

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