4.6 Article

Oct4 is Expressed in Human Gliomas and Promotes Colony Formation in Glioma Cells

Journal

GLIA
Volume 57, Issue 7, Pages 724-733

Publisher

WILEY-BLACKWELL
DOI: 10.1002/glia.20800

Keywords

Oct4; glioma; self-renewal; proliferation; Stat3

Categories

Funding

  1. Program for New Century Excellent Talents in University of China [NCET 04-0624]
  2. National Basic Research Program or China (973 Program) [2007CB512001, 2009CB941403]
  3. Natural Science Foundation of China [30671105, 30771142]

Ask authors/readers for more resources

There is increasing evidence that self-renewal capacity of cancer cells is critical for carcinogenesis; hence, it is vital to examine the expression and involvement of self-renewal regulatory genes in these cells. Here, we reported that Oct4, a well-known regulator of self-renewal in embryonic stem cells, was highly expressed in human gliomas and glioma cell lines, and the expression levels were increased in parallel with increasing glioma grades. In in vitro cell cultures, Oct4 was only expressed in rat C6 glioma cells and rat neural stem cells but not in rat brain differentiated cells. Downregulation of Oct4 expression by RNA interference in C6 cells was associated with reduced cell proliferation and colony formation. Further analysis revealed that Oct4 could upregulate phosphorylation of Stat3 to promote tumor cell proliferation. Overexpression of Oct4 in C6 cells increased the expression of nestin but decreased the expression of GFAP suggesting that Oct4 might inhibit the differentiation of glioma cells. Our findings may provide further evidence for the stem cell theory of carcinogenesis. In contrast, the results might also imply that Oct4 contributes to the existence of undifferentiated cells in gliomas. (C) 2008 Wiley-Liss, Inc.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.6
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available