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Biological characteristics of renal cancer cells after CTP-mediated cancer suppressor gene NPRL2 protein treatment

  • Yang Zeng , Xiao-Bo Shi , Zheng-Yong Yuan , Mao Ye , Li Jiang , Zhi-Xiong Chen , Jing Xiong and Wei Tang EMAIL logo
Published/Copyright: May 16, 2016

Abstract

Nitrogen permease regulator like-2 (NPRL2) has been proved to be a useful suppressor gene in treating many cancers containing renal cancer based on experiments. Transgenic technology which transfect exogenous NPRL2 gene into cancer cell was used in these experiments. However, this technology has defects, such as gene mutation and loss. Cytoplasmic transduction peptide (CTP) can be used to avoid these defects because it can directly mediate proteins to penetrate cell membrane and specifically locate in cytoplasm. In this article, CTP was used to directly mediate NPRL2 protein into the renal cancer cell line 786-O, then cell proliferation was detected by the CCK-8 method, cell cycle and apoptosis were detected by flow cytometry, cell invasion and migration ability were detected by the Transwell assay. Bcl-xl, Cyt-c and caspase-3 were detected by real-time fluorescent quantitative PCR and Western blot for the analysis of the related mechanism. The result showed that CTP successfully mediated NPRL2 protein into renal cancer cells and the growth of cells was significantly inhibited. The mechanism may be NPRL2 down-regulating the expression of Bcl-xl which can up-regulate Cyt-c and further activate caspase-3, and then a cascade reaction is caused for cell apoptosis on the classic mitochondrial apoptosis pathway.

Award Identifier / Grant number: cstc2013yykfA110004

Funding statement: This work was supported in part by the research grant from the Chongqing Science and Technology Commission (No. cstc2013yykfA110004).

Acknowledgments:

This work was supported in part by the research grant from the Chongqing Science and Technology Commission (No. cstc2013yykfA110004).

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Received: 2016-2-23
Accepted: 2016-5-12
Published Online: 2016-5-16
Published in Print: 2016-11-1

©2016 Walter de Gruyter GmbH, Berlin/Boston

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