AXIN1-related CSRNP1 mRNA expression and its transcriptional regulation in TGF-β1-induced tumor cells / 南方医科大学学报
Journal of Southern Medical University
; (12): 1122-1126, 2013.
Article
Dans Zh
| WPRIM
| ID: wpr-319464
Responsable en Bibliothèque :
WPRO
ABSTRACT
<p><b>OBJECTIVE</b>To investigate AXIN1-related CSRNP1 gene expression and the mechanism of its transcriptional regulation in TGF-β1-induced tumor cells.</p><p><b>METHODS</b>Human lung carcinoma A549 cells or human prostate cancer PC3 cells were treated with TGF-β1 at different doses (0, 20, 40, and 80 ng/ml) or at 20 ng/ml for 0, 8, 12, or 24 h, and the dose and time effect of TGF-β1 on CSRNP1 mRNA expression in the tumor cells were evaluated with real-time RT-PCR. A549 cells were also treated with TGF-β1 and cycloheximide to clarify whether CSRNP1 expression induced by TGF-β1 required de novo protein synthesis. A549 cells transfected with pcDNA3.1, flag-SMAD3, or flag-SMAD3-mu, after serum starvation, were treated with or without TGF-β1 (20 ng/mL) for 24 h, and the overexpression of wild-type SMAD3 and dominant negative SMAD3-mu mutant were confirmed by Western blotting. The effect of SMAD3 or SMAD3-mu overexpression on CSRNP1 mRNA expression was also measured by real-time RT-PCR.</p><p><b>RESULTS</b>In both A549 and PC3 cells, TGF-β1 dose- and time-dependently stimulated CSRNP1 expression, which required de novo protein synthesis in A549 cells. Overexpression of wild-type SMAD3 significantly increased the expression of CSRNP1 mRNA induced by TGF-β1, while overexpression of dominant negative SMAD3 mutant remarkably reduced CSRNP1 mRNA expression in response to TGF-β1 in A549 cells.</p><p><b>CONCLUSION</b>TGF-β1 may contribute to CSRNP1 expression through SMAD3 activation and downstream signaling in tumor cells.</p>
Texte intégral:
1
Indice:
WPRIM
Sujet Principal:
Pharmacologie
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ARN messager
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Transfection
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Transduction du signal
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Régulation de l'expression des gènes tumoraux
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Lignée cellulaire tumorale
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Protéine Smad-3
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Protéines régulatrices de l'apoptose
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Facteur de croissance transformant bêta-1
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Axine
Limites du sujet:
Humans
langue:
Zh
Texte intégral:
Journal of Southern Medical University
Année:
2013
Type:
Article