Comparison of Cellular Transforming Activity of OCT4, NANOG, and SOX2 in Immortalized Astrocytes

Sunyoung Seo, Hee Young Jeon, Hyunggee Kim

Research output: Contribution to journalArticle

1 Citation (Scopus)

Abstract

Embryonic stem cell factors - OCT4, NANOG, and SOX2 - contribute to the maintenance of stem cell properties and malignant progression in various cancers, including glioblastoma. Although functional roles of each of these genes are well documented in stem cell and cancer biology, no study has directly compared their cellular transforming activity under same experimental conditions. In this study, we compared the cellular transforming activity of OCT4, NANOG, and SOX2 using human immortalized astrocytes cultured under serum-free stem cell culture conditions. We found that SOX2 exhibited the strongest transforming activities, such as cell proliferation, neurosphere formation, resistance to cytotoxic drug, and cell migration/invasion, which may be associated with the activation of the nuclear factor kappa B (NFκB) signaling pathway. Thus, OCT4, NANOG, and SOX2, known to be frequently activated in various cancers and cancer stem cells, may play a distinct role in the regulation of cellular transformation.

Original languageEnglish
Pages (from-to)1000-1009
Number of pages10
JournalDNA and Cell Biology
Volume36
Issue number11
DOIs
Publication statusPublished - 2017 Nov 1

Fingerprint

Astrocytes
Stem Cells
Stem Cell Factor
Neoplastic Stem Cells
NF-kappa B
Glioblastoma
Embryonic Stem Cells
Cell Movement
Cell Biology
Neoplasms
Cell Culture Techniques
Maintenance
Cell Proliferation
Serum
Pharmaceutical Preparations
Genes

Keywords

  • astrocytes
  • cellular transformation
  • NANOG
  • NFκB
  • OCT4
  • SOX2

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Cell Biology

Cite this

Comparison of Cellular Transforming Activity of OCT4, NANOG, and SOX2 in Immortalized Astrocytes. / Seo, Sunyoung; Jeon, Hee Young; Kim, Hyunggee.

In: DNA and Cell Biology, Vol. 36, No. 11, 01.11.2017, p. 1000-1009.

Research output: Contribution to journalArticle

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