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The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
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Wnt is a zygotic effect gene that is expressed during very early embryonic development. It regulates various processes in animals starting from early development through the adult stage, such as organogenesis in the embryo and maintenance of neuronal and blood stem cells. Wnt proteins can induce a wide variety of intracellular pathways depending upon the specific abilities of different Wnt ligands to form a complex with shared and cognate receptors in the presence of different co-receptors. The...
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Related Experiment Video

Updated: Apr 6, 2026

Three-Dimensional Bone Extracellular Matrix Model for Osteosarcoma
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Wnt1-induced MAFK expression promotes osteosarcoma cell proliferation.

R Wang1, J Zheng1, D-S Zhang1

  • 1Department of Orthopedics, The 117th Hospital of PLA, Hangzhou, Zhejiang, China.

Genetics and Molecular Research : GMR
|July 28, 2015
PubMed
Summary

Musculoaponeurotic fibrosarcoma oncogene homolog K (MAFK) promotes osteosarcoma cell proliferation. Wnt1 signaling upregulates MAFK, driving tumor growth and cell cycle changes in osteosarcoma.

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Osteosarcoma is a prevalent bone tumor in pediatric and young adult populations.
  • Understanding the molecular mechanisms driving osteosarcoma proliferation is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the role of musculoaponeurotic fibrosarcoma oncogene homolog K (MAFK) in osteosarcoma cell proliferation.
  • To elucidate the signaling pathways involved in MAFK-mediated osteosarcoma development.

Main Methods:

  • Gene microarray assay to identify correlations between MAFK and signaling pathways.
  • In vitro studies using osteosarcoma cell lines (MG63) to assess MAFK expression and cell viability.
  • Treatment with Wnt1 and a Wnt pathway inhibitor (IWR-1-endo).
  • Cell cycle analysis to evaluate proliferation changes.

Main Results:

  • MAFK was found to be expressed at low levels in an osteosarcoma cell line.
  • A significant correlation was observed between MAFK and the Wnt signaling pathway.
  • Wnt1 dose-dependently induced MAFK expression, increasing cell viability.
  • Inhibition of the Wnt pathway abolished Wnt1-induced MAFK effects.
  • Enhanced cell proliferation was linked to cell cycle redistribution.

Conclusions:

  • Wnt1-induced MAFK expression promotes cell proliferation in osteosarcoma cells.
  • MAFK plays a significant role in osteosarcoma pathogenesis, closely associated with the Wnt signaling pathway.