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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 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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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.
The mTOR pathway or the...

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Related Experiment Video

Updated: May 18, 2026

A Blood-based Test for the Detection of ROS1 and RET Fusion Transcripts from Circulating Ribonucleic Acid Using Digital Polymerase Chain Reaction
10:35

A Blood-based Test for the Detection of ROS1 and RET Fusion Transcripts from Circulating Ribonucleic Acid Using Digital Polymerase Chain Reaction

Published on: April 5, 2018

MAP17, a ROS-dependent oncogene.

Amancio Carnero1

  • 1Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocío, Consejo Superior de Investigaciones Cientificas, Universidad de Sevilla Sevilla, Spain.

Frontiers in Oncology
|September 14, 2012
PubMed
Summary
This summary is machine-generated.

MAP17 protein overexpression enhances cancer cell proliferation, migration, and tumor growth by increasing reactive oxygen species (ROS). Targeting MAP17 may offer new strategies for cancer treatment and diagnosis.

Keywords:
MAP17canceroncogenereactive oxygen speciestumorigenesis

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Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis
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Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis

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Related Experiment Videos

Last Updated: May 18, 2026

A Blood-based Test for the Detection of ROS1 and RET Fusion Transcripts from Circulating Ribonucleic Acid Using Digital Polymerase Chain Reaction
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Published on: April 5, 2018

Identification and Characterization of Metastatic Factors by Gene Transfer into the Novel RIP-Tag; RIP-tva Murine Model
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Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis
09:45

Mosaic Zebrafish Transgenesis for Functional Genomic Analysis of Candidate Cooperative Genes in Tumor Pathogenesis

Published on: March 31, 2015

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • MAP17 is a small, non-glycosylated membrane protein identified as overexpressed in various carcinomas.
  • MAP17 overexpression in breast tumor cells correlates with an enhanced tumoral phenotype, including increased proliferation, migration, and resistance to apoptosis.

Purpose of the Study:

  • To investigate the role of MAP17 in promoting malignant cell behavior.
  • To elucidate the molecular mechanisms underlying MAP17-induced tumorigenesis.
  • To evaluate MAP17 as a potential biomarker for cancer progression.

Main Methods:

  • Overexpression of MAP17 in breast tumor cells.
  • Assessment of cellular proliferation, apoptosis, and migration.
  • Measurement of reactive oxygen species (ROS) production.
  • Mutation of the PDZ-binding domain of MAP17.
  • Tumorigenesis assays in nude mice.
  • Immunohistochemical analysis of MAP17 in human carcinomas.

Main Results:

  • MAP17 overexpression significantly enhanced tumor cell proliferation, migration, and resistance to apoptosis, leading to improved tumor growth in vivo.
  • MAP17-induced malignant phenotype was associated with increased ROS production.
  • Antioxidant treatment reduced the tumorigenic properties of MAP17-expressing cells.
  • Disruption of MAP17's PDZ-binding domain abolished its ability to increase ROS production and tumorigenesis.
  • MAP17 overexpression strongly correlated with tumoral progression in human carcinomas.

Conclusions:

  • MAP17 promotes a malignant cell phenotype through increased ROS production, dependent on its PDZ-binding domain.
  • MAP17 is a significant factor in cancer progression across various human carcinomas.
  • MAP17 serves as a potential biomarker for tumorigenesis and malignant progression.