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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.
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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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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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Rous Sarcoma virus or RSV was discovered by F. Peyton Rous in the year 1911 as a filterable transmissible agent that could cause tumors in chickens. He won a Nobel Prize for this discovery in 1966. His experiments clearly demonstrated that some cancers could be caused by infectious agents and led to the discovery of many more cancer-causing viruses in animals as well as humans.
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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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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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Updated: Oct 9, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
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Alternative polyadenylation is a determinant of oncogenic Ras function.

Aishwarya Subramanian1, Mathew Hall2, Huayun Hou3

  • 1Developmental and Stem Cell Biology Program, Peter Gilgan Centre for Research and Learning, The Hospital for Sick Children, Toronto, ON M5G 0A4, Canada.

Science Advances
|December 17, 2021
PubMed
Summary
This summary is machine-generated.

Alternative polyadenylation, regulated by CFIM-1, impacts Ras oncogene function in development and cancer. Its disruption affects cell migration and epithelial-to-mesenchymal transition, highlighting a conserved role in cancer progression.

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Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Cancer Research

Background:

  • Alternative polyadenylation (APA) of mRNA plays crucial roles in biological development and cancer, though its precise functions remain unclear.
  • Activating mutations in the Ras oncogene are key drivers in numerous human cancers.
  • The Ras pathway is a critical signaling pathway involved in cell growth, differentiation, and survival.

Purpose of the Study:

  • To investigate the role of alternative polyadenylation machinery in the context of oncogenic Ras signaling.
  • To identify novel regulators of Ras function through genetic screening in Caenorhabditis elegans.
  • To explore the functional consequences of altered APA in cancer cells with Ras mutations.

Main Methods:

  • Conducted a genetic screen in Caenorhabditis elegans to identify enhancers of activated Ras (let-60).
  • Utilized gene ablation in C. elegans and gene depletion in human cancer cells to study the function of cfim-1/CFIm25.
  • Performed functional analysis of conserved transcripts affected by APA, including studies on vulva development and cell migration.

Main Results:

  • Identified cfim-1, a subunit of the APA machinery, as an enhancer of let-60/Ras gain-of-function in C. elegans.
  • Depletion of human CFIm25 in KRAS-mutant cancer cells promoted migration and epithelial-to-mesenchymal transition.
  • Observed biased poly(A) tail placement to proximal sites in conserved transcripts in cfim-1 mutants and CFIm25-depleted cells.
  • Identified mrp-5/ABCC1 as a novel regulator of C. elegans vulva development and human cell migration via alternative 3′ untranslated region (3′UTR) usage.

Conclusions:

  • Alternative polyadenylation, mediated by CFIM-1/CFIm25, plays a conserved role in regulating oncogenic Ras function.
  • Disruption of APA impacts key cellular processes such as cell migration and epithelial-to-mesenchymal transition, relevant to cancer progression.
  • APA represents a potential therapeutic target for cancers driven by Ras pathway mutations.