Oncotarget

Research Papers:

Frizzled-7 promoter is highly active in tumors and promoter-driven Shiga-like toxin I inhibits hepatocellular carcinoma growth

Hongpan Xu _, Lailing Gong, Yanyan Xia, Lili Qu, Qiwen Li, Lu Pang, Jin Si and Zhiyang Li

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Oncotarget. 2015; 6:39908-39923. https://doi.org/10.18632/oncotarget.5516

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Abstract

Hongpan Xu1,*, Lailing Gong1,*, Yanyan Xia1, Lili Qu1, Qiwen Li1, Lu Pang1, Jin Si1,2, Zhiyang Li1

1Department of Laboratory Medicine, the Second Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu 210011, China

2Department of Laboratory Medicine, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Nanjing, Jiangsu 210008, China

*These authors have contributed equally to this work

Correspondence to:

Jin Si, e-mail: [email protected]

Zhiyang Li, e-mail: [email protected]

Keywords: Frizzled-7 promoter, pFZD7-GFP, Shiga-like toxin I, pFZD7-Stx1, gene therapy

Received: May 09, 2015     Accepted: October 06, 2015     Published: October 16, 2015

ABSTRACT

Frizzled-7 protein plays a significant role in the formation of several malignant tumors. Up regulation of the Frizzled-7 in cancer cell lines is associated with nuclear accumulation of wild-type β-catenin from the Wnt/β-catenin pathway which is frequently activated in tumors. To analyze activity of the Frizzled-7 promoter in tumor cells, we constructed two recombinant plasmid vectors in which the Frizzled-7 promoter was used to drive the expression of green fluorescent protein (GFP) and Shiga-like toxin I (Stx1) (pFZD7-GFP/Stx1) genes. The Frizzled-7 protein was found to be expressed in the cancer cell lines but not in the normal cell lines. The GFP expression was restricted to the cancer cell lines and xenografts in the BALB/C mice but not to normal cell lines. Moreover, cell proliferation and tumor growth decreased significantly after transfection with the pFZD7-Stx1. Results from this study will help determine a highly effective strategy for gene therapy of tumors.


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