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Molecular Medicine Reports
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July 2013 Volume 8 Issue 1

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Article

Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression

  • Authors:
    • Hua Shi
    • Jun-Hong Deng
    • Zhu Wang
    • Kai-Yuan Cao
    • Liang Zhou
    • Hua Wan
  • View Affiliations / Copyright

    Affiliations: Department of Urology, The First People's Hospital Affiliated to Guangzhou Medical University, Guangzhou 510180, P.R. China, Research Center for Clinical Laboratory Standard, Department of Medical Microbiology, Zhongshan Medical School of Sun Yat-sen University, Guangzhou 510080, P.R. China
  • Pages: 35-40
    |
    Published online on: May 10, 2013
       https://doi.org/10.3892/mmr.2013.1470
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Abstract

Clusterin (CLU) is a glycoprotein involved in tumor progression, whose expression level correlates with the metastasis of renal cell carcinoma (RCC). However, the mechanism by which CLU plays an oncogenic role in RCC remains unclear. In this study, we used the human renal cancer cell 786-O as an experimental model. We knocked down CLU expression in the 786-O cells using lentiviral vector-mediated delivery of RNAi, and then compared the gene expression profiles between the knocked down CLU 786-O cells and control cells. We observed that CLU knockdown induced apoptosis and inhibited the proliferation and migration of 786-O cells. Microassay analysis revealed changes in the expression of 588 genes between the 786-O cells infected by a si-CLU lentivirus and the control cells, where 356 genes were upregulated and 232 were downregulated. Pathway analysis classified the differentially expressed genes into 17 upregulated and 12 downregulated pathways, including the PI3K/Akt, MAPK and VEGF pathways. In this study, we demonstrated that CLU acts as an oncogene in RCC by promoting cell proliferation and migration and inhibiting apoptosis. Microassay analysis may provide a platform for further characterization of the individual genes implicated in the development of RCC, providing new insights into the oncogenic role of CLU.
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Copy and paste a formatted citation
Spandidos Publications style
Shi H, Deng J, Wang Z, Cao K, Zhou L and Wan H: Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression. Mol Med Rep 8: 35-40, 2013.
APA
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., & Wan, H. (2013). Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression. Molecular Medicine Reports, 8, 35-40. https://doi.org/10.3892/mmr.2013.1470
MLA
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., Wan, H."Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression". Molecular Medicine Reports 8.1 (2013): 35-40.
Chicago
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., Wan, H."Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression". Molecular Medicine Reports 8, no. 1 (2013): 35-40. https://doi.org/10.3892/mmr.2013.1470
Copy and paste a formatted citation
x
Spandidos Publications style
Shi H, Deng J, Wang Z, Cao K, Zhou L and Wan H: Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression. Mol Med Rep 8: 35-40, 2013.
APA
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., & Wan, H. (2013). Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression. Molecular Medicine Reports, 8, 35-40. https://doi.org/10.3892/mmr.2013.1470
MLA
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., Wan, H."Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression". Molecular Medicine Reports 8.1 (2013): 35-40.
Chicago
Shi, H., Deng, J., Wang, Z., Cao, K., Zhou, L., Wan, H."Knockdown of clusterin inhibits the growth and migration of renal carcinoma cells and leads to differential gene expression". Molecular Medicine Reports 8, no. 1 (2013): 35-40. https://doi.org/10.3892/mmr.2013.1470
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