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Related Concept Videos

Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Rous Sarcoma Virus (RSV) and Cancer01:03

Rous Sarcoma Virus (RSV) and Cancer

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.
RSV is a retrovirus that contains two copies of a plus-strand  RNA genome. Its genome consists of four main open...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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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The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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The Ras Gene02:38

The Ras Gene

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Ras is a superfamily...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

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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Related Experiment Video

Updated: May 9, 2026

Modeling Astrocytoma Pathogenesis In Vitro and In Vivo Using Cortical Astrocytes or Neural Stem Cells from Conditional, Genetically Engineered Mice
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GRIM-19 mutations fail to inhibit v-Src-induced oncogenesis.

S Kalakonda1, S C Nallar1, D J Lindner2

  • 1Department of Microbiology & Immunology, Program in Oncology, Greenebaum Cancer Center, University of Maryland School of Medicine, Baltimore, MD, USA.

Oncogene
|July 16, 2013
PubMed
Summary

Mutations in the GRIM-19 gene in head and neck cancers inactivate its tumor-suppressing function against the oncogene v-Src. Wild-type GRIM-19 inhibits v-Src

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Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model
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Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model

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Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model
09:03

Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model

Published on: October 16, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • The non-receptor tyrosine kinase Src plays a key role in cell growth, survival, and differentiation, with its dysregulation implicated in human cancers.
  • The oncogenic mutant v-Src promotes cell survival, migration, invasion, and division, contributing to tumor progression.
  • GRIM-19 (Genes associated with Retinoid-IFN-induced Mortality 19) is an antioncogene that inhibits STAT3's pro-oncogenic effects, but its role concerning v-Src was unclear.

Purpose of the Study:

  • To investigate the mechanism by which GRIM-19 inhibits the pro-oncogenic effects of v-Src.
  • To identify and characterize GRIM-19 mutations in head and neck cancer patients and assess their functional impact.
  • To elucidate the role of GRIM-19 in regulating Src activity and its downstream targets like Pag1.

Main Methods:

  • Identification of GRIM-19 mutations in head and neck cancer patient samples.
  • Functional assays assessing the ability of wild-type and mutant GRIM-19 to inhibit v-Src-induced cell migration, cytoskeletal remodeling, and metastasis.
  • Evaluation of GRIM-19's effect on drug resistance in v-Src-transformed cells.
  • Analysis of Pag1 expression levels in response to wild-type and mutant GRIM-19 and v-Src.

Main Results:

  • Functionally inactivating mutations in GRIM-19 were identified in head and neck cancer patients.
  • Wild-type GRIM-19 inhibited v-Src-induced cell migration, cytoskeletal remodeling, and metastasis, whereas tumor-derived GRIM-19 mutants (L71P, L91P, A95T) failed to do so.
  • Mutant GRIM-19 proteins were unable to inhibit drug resistance in v-Src-transformed cells.
  • v-Src downregulated Pag1 expression, an inhibitor of Src; wild-type GRIM-19 restored Pag1 levels, but the mutants did not.

Conclusions:

  • GRIM-19 inhibits the pro-oncogenic effects of v-Src independently of STAT3, through a novel mechanism involving Pag1 regulation.
  • Mutations in GRIM-19 found in head and neck cancers lead to loss of its tumor-suppressive functions.
  • These findings reveal a new pathway by which Src activity is deregulated in cancer cells, highlighting GRIM-19 as a potential therapeutic target.