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Secreted protein acidic and rich in cysteine inhibits the growth of human pancreatic cancer cells with G1 arrest induction

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Tumor Biology

Abstract

Aberrant secreted protein acidic and rich in cysteine (SPARC) expression has been reported to play an important role in the tumor development. However, the pattern and the role of SPARC in pancreatic cancer remain largely unknown. Therefore, we further deciphered the role of SPARC played in pancreatic cancer. We first evaluated the SPARC expression in human pancreatic cancer tissues and pancreatic cancer cells. Then we forced expression and silenced SPARC expression in pancreatic cancer cell lines MIA PaCa2 and PANC-1, respectively, using lentivirus vectors. We characterized the stable cells in vitro. In this study, we found that SPARC expression was weak in cancer cells in specimens which negatively correlated with the expression level of phosphorylated pRB and poorer outcome. Moreover, our results demonstrated that SPARC negatively regulated pancreatic cell growth in vitro. Furthermore, we disclosed that the activation of p53 and p27Kip1 may involve in the effect of SPARC on pancreatic cancer cells. SPARC is downregulated in pancreatic cancer cells and retards the growth of pancreatic cancer cell. Taken together, these results indicate SPARC may be a potential target for pancreatic cancer therapy.

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Acknowledgments

This work was sponsored by The Natural Science Foundation of Jiangsu Province (Youth Fund), grant number: BK20130475, Zhenjiang Science and Technology Pillar Program, grant numbers: SH2012030 and SH2012031, The Foundation for Young Scientists of affiliated Hospital of Jiangsu University (grant number: JDFYRC2013009), and post-doctoral research funding schemes of Jiangsu Province (grant number: 1302096B)

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Correspondence to Xuqing Wang.

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Zhengfa Mao and Xiaoyan Ma equally contributed to this work.

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Mao, Z., Ma, X., Fan, X. et al. Secreted protein acidic and rich in cysteine inhibits the growth of human pancreatic cancer cells with G1 arrest induction. Tumor Biol. 35, 10185–10193 (2014). https://doi.org/10.1007/s13277-014-2315-0

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  • DOI: https://doi.org/10.1007/s13277-014-2315-0

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