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[Studies on the target cells and molecules with sodium valproate induced differential of human glioma cells]
Ai-dong Wang1, Xiao-yan Ji, Qiang Huang
1Department of Neurosurgery and Brain Tumor Laboratory, the Second Affiliated Hospital of Suzhou University, Suzhou 215004, China.
Objective:
To investigate the target cells and molecules with sodium valproate induced differentiation of human glioma cells.
Methods:
Nude mice bearing human glioma xenogenic graft subcutaneously were treated with sodium valproate. The expressions of HDAC1 and Tob genes of xenografts were analyzed with semiquantitative RT-PCR. The CD133+ cells (BTSCs) were isolated from glioma specimens by immunomagnetic sorting, and cultured in the medium containing FCS or in the serum-free medium supplemented with growth factors, respectively, followed by treatment with sodium valproate in vitro for 21 days. The cell surface markers were detected with flow cytometry and confocal microscopy.
Results:
Sodium valproate inhibited the growth of subcutaneous xenografs bearing on nude mice (P<0.05), and up-regulated the HDAC1 expression (P<0.01), down-regulated the Tob expression (P<0.05). The cell surface markers of BTSCs were detected by flow cytometry after sodium valproate treatment for 21 days. In the FCS group, the GFAP or beta-tubulin III positive cells increased significantly (P<0.01), but in the growth factor group, no statistical differences were observed in the GFAP or beta-tubulin III expression (P>0.05). The results of confocal microscopy indicated that the GFAP+ or beta-tubulin III+ cells coexpressed with Nestin.
Conclusions:
HDAC1 and Tob genes were the potential target molecules in reversion of the differential inhibition of human glioma cells with sodium valproate. The BTSCs undergoing the processes of differentiation were the target cells for sodium valproate.
Insights
Sodium valproate targets brain tumor stem cells (BTSCs) for differentiation, modulating HDAC1 and Tob gene expression. This study identifies key molecules and cells involved in glioma treatment.
Area of Science:
- Neuro-oncology
- Molecular Biology
- Cancer Stem Cell Research
Background:
- Human glioma cells exhibit potential for differentiation.
- Sodium valproate is an established therapeutic agent with potential anti-cancer properties.
Purpose of the Study:
- To investigate the molecular targets and cellular mechanisms of sodium valproate-induced differentiation in human glioma cells.
- To identify potential therapeutic targets for glioma treatment.
Main Methods:
- Sodium valproate treatment of human glioma xenografts in nude mice.
- Analysis of HDAC1 and Tob gene expression using semiquantitative RT-PCR.
- Isolation and in vitro culture of CD133+ cells (brain tumor stem cells - BTSCs) with subsequent sodium valproate treatment.
- Detection of cell surface markers using flow cytometry and confocal microscopy.
Main Results:
- Sodium valproate inhibited xenograft growth and modulated HDAC1 and Tob gene expression.
- In vitro, sodium valproate treatment of BTSCs in FCS medium significantly increased GFAP and beta-tubulin III positive cells.
- Confocal microscopy confirmed coexpression of GFAP/beta-tubulin III with Nestin in differentiated BTSCs.
Conclusions:
- HDAC1 and Tob genes are potential molecular targets for sodium valproate in reversing differentiation inhibition of human glioma cells.
- Brain tumor stem cells (BTSCs) undergoing differentiation are the primary cellular targets for sodium valproate's therapeutic effects.
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