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Regulation of tumorigenesis in oral epithelial cells by defined reprogramming factors Oct4 and Sox2

Jinghua Cai1, Baoxia He2, Xinming Li1

  • 1Department of Stomatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, P.R. China.

Oncology Reports
|June 10, 2016
PubMed

Insights

Oct4 and Sox2 overexpression drives oral cancer stem cell reprogramming and tumor formation. Knocking down Sox2 reduced tumor size, while Oct4 knockdown alone increased oral cancer aggressiveness.

Area of Science:

  • Oncology
  • Stem Cell Biology
  • Molecular Biology

Background:

  • Oct4 and Sox2 are key pluripotent stem cell factors.
  • Their interplay in tumorigenesis, particularly oral carcinogenesis, remains largely unelucidated.
  • Understanding these factors is crucial for targeting cancer stem cells.

Purpose of the Study:

  • To investigate the roles of Oct4 and Sox2 in the reprogramming of oral cancer stem cells.
  • To determine the effect of Oct4 and Sox2 manipulation on oral cancer development and progression.

Main Methods:

  • Overexpression of Oct4 and/or Sox2 in immortalized oral epithelial cells (hTERT+-OME) via lentivirus transduction.
  • Knockdown of Oct4 and/or Sox2 in oral squamous cell carcinoma (OSCC) cell lines (Cal27 and primary OSCC) using shRNA.
  • Assessment of tumor formation and xenograft growth in immunodeficient mice.

Main Results:

  • Co-overexpression of Oct4 and Sox2 (Oct4+Sox2+) in hTERT+-OME cells led to tumor formation in immunodeficient mice.
  • Single overexpression of Oct4+ or Sox2+ did not induce tumor formation.
  • Knockdown of Sox2 (Sox2low) or both Oct4 and Sox2 (Oct4lowSox2low) decreased tumor size.
  • Single knockdown of Oct4 (Oct4low) resulted in more aggressive xenografts.

Conclusions:

  • The combination of Oct4 and Sox2 is critical for inducing tumorigenesis from reprogrammed oral epithelial cells.
  • Oct4 and Sox2 play distinct roles in oral cancer stem cell behavior and tumor progression.
  • Oct4+Sox2+ cells are implicated as reprogrammed cancer stem cells driving oral carcinogenesis.

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