4.7 Article

Quantitative Proteomics of TRAMP Mice Combined with Bioinformatics Analysis Reveals That PDGF-B Regulatory Network Plays a Key Role in Prostate Cancer Progression

期刊

JOURNAL OF PROTEOME RESEARCH
卷 17, 期 7, 页码 2401-2411

出版社

AMER CHEMICAL SOC
DOI: 10.1021/acs.jproteome.8b00158

关键词

PDGF-B; proteomics; prostate cancer; bioinformatics analysis; TRAMP mice; signal pathway

资金

  1. Taishan Scholars Construction Engineering, National Natural Science Foundation of China [31671139, 81670855, 31771284, 81672093]
  2. Shandong Provincial Natural Science Foundation [ZR2016JL026]
  3. Key Research and Development Plan of Shandong Province [2018GSF118131, 2017GSF18103, 2017GSF18121, 2016GSF201100]
  4. Shandong Province Higher Educational Science and Technology Program [J15LK03]
  5. Yantai Science and Technology Plan [2015ZH086]
  6. Swedish Research Council [621-2011-4423, 2015-4870]

向作者/读者索取更多资源

Transgenic adenocarcinoma of the mouse prostate (TRAMP) mice is a widely used transgenic animal model of prostate cancer (PCa). We performed a label-free quantitative proteomics analysis combined with a bioinformatics analysis on the entire prostate protein extraction from TRAMP mice and compared it with WT littermates. From 2379 total identified proteins, we presented a modest mice prostate reference proteome containing 919 proteins. 61 proteins presented a significant expression difference between two groups. The integrative bioinformatics analysis predicted the overexpression of platelet-derived growth factor B (PDGF-B) in tumor tissues and supports the hypothesis of the PDGF-B signaling network as a key upstream regulator in PCa progression. Furthermore, we demonstrated that Crenolanib, a novel PDGF receptor inhibitor, inhibited PCa cell proliferation in a dose-dependent manner. Finally, we revealed the importance of PDGF-B regulatory network in PCa progression, which will assist us in understanding the role and mechanisms of PDGF-B in promoting cancer growth and provide valuable knowledge for future research on anti-PDGF therapy.

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