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Related Concept Videos

The Ras Gene02:38

The Ras Gene

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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.
Ras is a...
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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.
Three regulatory proteins control their activity:
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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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MAPK Signaling Cascades01:07

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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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Interactions Between Signaling Pathways01:19

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
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Plakins are large proteins with binding domains for microtubules, microfilaments, intermediate filaments, and membrane-associated protein complexes at cell junctions. Plakin functions are evolutionarily conserved and are primarily involved in organizing the different components of the cytoskeleton by crosslinking them to each other and connecting them to the cell-matrix and cell adhesion complexes. They are also known to interact with signal transducers, serve as scaffolds for signaling...
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The metastasis-promoting P1597L mutation in PlexinB1 enhances Ras activity.

Ritu Garg1, Magali Williamson2

  • 1School of Cancer and Pharmaceutical Sciences, Faculty of Life Sciences & Medicine, King's College London, Room 2.34B, New Hunts House, London, SE1 1UL, UK.

BMC Cancer
|August 13, 2024
PubMed
Summary
This summary is machine-generated.

A specific mutation (Proline1597Leucine) in PlexinB1 transforms it from a prostate cancer suppressor to a metastasis driver by activating Ras signaling. This highlights the PlexinB1-Rap-Ras pathway as a potential therapeutic target.

Keywords:
MetastasisMutationPlexinProstate cancerRapGTPaseRas

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Signaling

Background:

  • Metastatic prostate cancer poses a significant health burden, with underlying molecular drivers often unclear.
  • Plexins, semaphorin receptors, have varied roles in cancer; a specific mutation (P1597L) in PlexinB1 is linked to prostate cancer metastasis.
  • The mechanism by which PlexinB1(P1597L) promotes metastasis remains unknown.

Purpose of the Study:

  • To elucidate the molecular mechanism by which the PlexinB1(P1597L) mutation promotes prostate cancer metastasis.
  • To investigate the impact of the P1597L mutation on PlexinB1's interaction with small GTPases and its signaling pathways.

Main Methods:

  • GST pulldown assays to assess Rap and Ras activity, and protein-protein interactions.
  • Immunoblotting for Akt/ERK phosphorylation and cycloheximide treatment for protein stability.
  • Monitoring Rho/ROCK activity via MLC2 phosphorylation and cell-collapse assays to evaluate PlexinB1 function.

Main Results:

  • The P1597L mutation converts PlexinB1 from a Ras repressor to an activator by inhibiting its RapGAP activity, leading to increased Ras activity.
  • The mutation blocks PlexinB1-mediated Rho/ROCK inhibition, preserving Rho signaling and actin stress fibers.
  • PlexinB1(P1597L) does not significantly alter interactions with small GTPases or RTKs, nor does it affect Akt/ERK phosphorylation, indicating a specific effect on Rho signaling via Rap/Ras.

Conclusions:

  • The P1597L mutation in PlexinB1 drives prostate cancer metastasis by activating Ras signaling through reduced RapGAP activity.
  • This study identifies the PlexinB1-Rap-Ras pathway as a critical mediator of prostate cancer progression.
  • Targeting the PlexinB1-Rap-Ras pathway offers a potential therapeutic strategy for metastatic prostate cancer.