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Related Concept Videos

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Bone formation, or ossification, begins around the sixth to seventh week of embryonic development. Most bones develop from a cartilaginous template through the process of endochondral ossification. Cartilage formation begins when clusters of mesenchymal cells differentiate into chondrocytes. These chondrocytes proliferate rapidly and secrete an extracellular matrix that becomes encased in a membrane called the perichondrium. The resulting cartilage model provides a template that resembles the...
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Chondrogenic Differentiation Induction of Adipose-derived Stem Cells by Centrifugal Gravity
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cFOS-SOX9 Axis Reprograms Bone Marrow-Derived Mesenchymal Stem Cells into Chondroblastic Osteosarcoma.

Yunlong He1, Wentao Zhu2, Min Hwa Shin1

  • 1Cancer and Stem Cell Epigenetics Section, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute, Building 37, Room 3140A, Bethesda, MD 20892, USA.

Stem Cell Reports
|May 30, 2017
PubMed
Summary

Oncogenes dictate osteosarcoma subtypes originating from bone marrow-derived mesenchymal stem cells (BMSCs). The cFOS-SOX9 pathway is crucial for developing chondroblastic osteosarcoma.

Keywords:
AKTRASSOX9cFOScancercancer stem cellsmesenchymal stem cellsosteosarcomap53stem cells

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Establishment of Cancer Stem Cell Cultures from Human Conventional Osteosarcoma
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Area of Science:

  • Oncology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Bone marrow-derived mesenchymal stem cells (BMSCs) are implicated as the cell of origin for various osteosarcoma (OS) subtypes.
  • The specific signaling pathways that guide BMSCs toward different OS subtypes remain largely undefined.

Purpose of the Study:

  • To elucidate the oncogenic signals that determine the subtype of osteosarcoma (OS) arising from bone marrow-derived mesenchymal stem cells (BMSCs).
  • To investigate the molecular mechanism by which cFOS induces chondroblastic OS formation.

Main Methods:

  • Spontaneous transformation of p53 knockout (p53_KO) BMSCs.
  • Introduction of oncogenes (RAS, AKT, cFOS) to assess their impact on BMSC transformation.
  • Integrated genome-wide studies to identify regulatory mechanisms.
  • Analysis of cFOS binding to the Sox9 promoter and SOX9's role in chondroblastic OS.

Main Results:

  • Loss of p53 in BMSCs defaults to osteoblastic OS.
  • RAS, AKT, and cFOS oncogenes override the default pathway, leading to undifferentiated sarcoma, enhanced osteoblastic OS, and chondroblastic OS, respectively.
  • cFOS directly binds to the Sox9 promoter, inducing its transcription in BMSCs.
  • SOX9 is essential for cFOS-mediated cartilage formation in chondroblastic OS.

Conclusions:

  • Oncogenic signals play a critical role in determining the specific subtype of osteosarcoma derived from BMSCs.
  • The cFOS-SOX9 signaling axis is a key determinant for the development of chondroblastic osteosarcoma.