Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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...
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Role of Hematopoietic Growth Factors01:28

Role of Hematopoietic Growth Factors

Hematopoietic growth factors are molecules that regulate the differentiation rate of hematopoietic stem cells (HSCs). Erythropoietin (EPO), primarily produced by the kidneys, plays a crucial role in erythrocyte production. When oxygen levels in the blood are low, EPO is released into the bloodstream, reaching the bone marrow, where it stimulates HSCs to differentiate and mature into erythrocytes, which are vital for oxygen transport.
Thrombopoietin (TPO), mainly released by the liver,...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Clinical determinants, diagnostic complexity, and molecular heterogeneity in NF1-associated and sporadic malignant peripheral nerve sheath tumors: A 25-year referral-center cohort.

European journal of cancer (Oxford, England : 1990)·2026
Same author

Myxoid neoplasms with MAP3K kinase fusion: a study of 39 cases.

Histopathology·2026
Same author

Alternative lengthening of telomeres and CINSARC are interconnected toward non-translocation-related sarcomas progression.

BMC cancer·2026
Same author

Tetraploidy in cancer: Diagnostic and therapeutic perspectives.

Biochemical pharmacology·2026
Same author

Transcriptomic comparative study between canalicular adenoma and HMGA2::WIF1 canalicular-like pleomorphic adenoma.

The Journal of pathology·2026
Same author

Expanding the Spectrum of Ubiquitin-specific Proteases-Fused Neoplasms: A Clinicopathologic and Molecular Study of USP2- and USP8-Rearranged Spindle Cell Tumors.

The American journal of surgical pathology·2026

Related Experiment Video

Updated: May 18, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
03:36

Development of Compendium for Esophageal Squamous Cell Carcinoma

Published on: April 12, 2024

Oncostatin M is a growth factor for Ewing sarcoma.

Emmanuelle David1, Franck Tirode, Marc Baud'huin

  • 1INSERM, UMR, Ligue Team 2012, Nantes, France.

The American Journal of Pathology
|September 18, 2012
PubMed
Summary

Oncostatin M (OSM) promotes Ewing sarcoma (ES) growth by activating specific receptors and MYC, unlike in other bone tumors. This finding offers new therapeutic avenues for rare bone malignancies.

More Related Videos

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis
12:03

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis

Published on: December 9, 2016

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
07:31

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

Related Experiment Videos

Last Updated: May 18, 2026

Development of Compendium for Esophageal Squamous Cell Carcinoma
03:36

Development of Compendium for Esophageal Squamous Cell Carcinoma

Published on: April 12, 2024

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis
12:03

In Vivo Model for Testing Effect of Hypoxia on Tumor Metastasis

Published on: December 9, 2016

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate
07:31

A Syngeneic Orthotopic Osteosarcoma Sprague Dawley Rat Model with Amputation to Control Metastasis Rate

Published on: May 3, 2021

Area of Science:

  • Molecular oncology
  • Cell signaling in cancer

Background:

  • Primary bone tumors like osteosarcomas and chondrosarcomas originate from mesenchymal stem cells.
  • Ewing sarcomas (ESs) involve the EWS-FLI1 fusion protein, inhibiting mesenchymal differentiation and promoting neuroectodermic features.
  • Oncostatin M (OSM), an IL-6 family cytokine, has complex effects on cell proliferation and differentiation, with MYC acting as a potential molecular switch.

Purpose of the Study:

  • To investigate the differential effects of OSM on various bone tumor cell lines.
  • To elucidate the molecular mechanisms underlying OSM-induced proliferation in Ewing sarcomas.
  • To explore the role of EWS-FLI1 in maintaining stemness and neuroectodermic features in ES.

Main Methods:

  • Comparison of OSM's effects on osteosarcoma, chondrosarcoma, and Ewing sarcoma cell lines.
  • Knockdown experiments to assess the dependence of OSM-induced growth on specific receptors (LIFR, OSMR), STAT3, and MYC.
  • Analysis of gene expression profiles in ES cell lines, xenografts, and patient samples.

Main Results:

  • OSM induced proliferation in ES cell lines, whereas it was cytostatic in osteosarcomas and chondrosarcomas.
  • OSM-driven ES cell growth required both Type I (LIFR) and Type II (OSMR) receptors, high STAT3 activation, and elevated MYC expression.
  • ES cell lines, xenografts, and patient samples exhibited low LIF, high LIFR/OSMR ratio, and high MYC expression, consistent with neuroectodermic features maintained by EWS-FLI1.

Conclusions:

  • The EWS-FLI1 fusion protein in Ewing sarcomas maintains stemness and neuroectodermic characteristics, leading to a unique response to OSM.
  • The high LIFR/OSMR ratio and elevated MYC expression are key features of ES driven by EWS-FLI1.
  • Understanding these mechanisms in rare bone tumors provides insights into broader cancer regulation and potential therapeutic targets.