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. 2013 Aug 5:8:132.
doi: 10.1186/1746-1596-8-132.

Effect of STAT5 silenced by siRNA on proliferation apoptosis and invasion of esophageal carcinoma cell line Eca-109

Qian Yang  1 , Min Li, Tao Wang, Hong Xu, Wenqiao Zang, Guoqiang Zhao
Affiliations

Effect of STAT5 silenced by siRNA on proliferation apoptosis and invasion of esophageal carcinoma cell line Eca-109

Qian Yang et al. Diagn Pathol. .

Abstract

Background: STAT is the backward position of cytokine and growth factor receptors in the nucleus, STAT dimers could bind to DNA and induce transcription of specific target genes. Several lines of evidence support the important roles of STAT, especially STAT5, in carcinogenesis. The overexpression of STAT 5 is related to the differentiation and apoptosis of tumor cells. However, the role of STAT5 in esophageal squamous cell carcinoma remains unclear.

Methods: The siRNA vectors aiming to STAT5 gene were constructed. STAT5 siRNA was transfected into Eca-109 cells by Lipofectamine™2000. Expression of STAT5、Bcl-2 and Cyclin D1 were analyzed by Western blot and RT-PCR. Eca-109 cells proliferation was determined by MTT. Eca-109 cell cycle and apoptosis were detected by the flow cytometry. Boyden chamber was used to evaluate the invasion and metastasis capabilities of Eca-109 cells.

Results: The double strands oligonucleotide of siRNA aiming to STAT5 was successfully cloned into the pRNAT-U6.1 vector, and the target sequence coincided with the design. RT-PCR and Western blotting detection demonstrated that the expression levels of STAT5、Bcl-2 and Cyclin D1 gene were obviously decreased in Eca-109 cells transfected with STAT5 siRNA. STAT5 siRNA could suppress the proliferation of Eca-109 cells. The proportion of S and G2/M period frequency was significantly decreased (p<0.05). The proportion of G0/G1 period frequency was significantly increased (p<0.05). The average amount of cells penetrating Matrigel was significantly decreased (p<0.05).

Conclusions: STAT5 silenced by siRNA could induce the apoptosis and suppress the proliferation、invasion and metastasis of esophageal carcinoma cell line Eca-109, which indicated STAT5 might be a novel therapeutic strategy for the human ESCC.

Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1351913072103000.

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Figures

Figure 1
Figure 1
The results of protein expression and cell proliferation. A STAT5 siRNA inhibited significantly the protein expression of STAT5、Bcl-2 and Cyclin D1. Cells were incubated with different synthetic oligonucleotides as described in the materials and methods section, and CXCR4 protein was quantified by Western-Blot. The targeted CXCR4 siRNA inhibited significantly the protein expression of STAT5、Bcl-2 and Cyclin D1 gene. B cell proliferation was assessed using the MTT assay. Data are presented as the mean of four experiments. Silencing the STAT5 depresses the proliferation of esophageal carcinoma cell line Eca-109. Significant difference (p <0.05).
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