Yi Wang

Wenzhou University, Yung-chia, Zhejiang Sheng, China

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Publications (3)6.46 Total impact

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    ABSTRACT: Ribosomal protein s15a (RPS15A) is a highly conserved protein that promotes mRNA/ribosome interactions early in translation. Recent evidence showed that RPS15A could stimulate the growth in yeast, plant and human lung carcinoma. Here we report that RPS15A knockdown could inhibit hepatic cancer cell growth in vitro. When transduced with shRPS15A-containing lentivirus, we observed inhibited cell proliferation and impaired colony formation in both HepG2 and Bel7404 cells. Furthermore, cell cycle analysis showed that HepG2 cells were arrested at G0/G1 phase when transduced with Lv-shRPS15A. In conclusion, our findings provide for the first time the biological effects of RPS15A in hepatic cancer cell growth. RPS15A may play a prominent role in heptocarcinogenesis and serve as a potential therapeutic target in hepatocellular carcinoma.
    No preview · Article · Dec 2013 · Gene
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    ABSTRACT: Kruppel-like factor 8 (KLF8) is a transcription factor which has been identified to play a critical role in oncogenic transformation, epithelial-mesenchymal transition and invasion. Higher expression level of KLF8 has been observed in ovarian, renal and breast cancer cells. This study focused on investigating the knockdown effects of KLF8 through lentivirus mediated targeted disruption of KLF8 in gastric cancer cell lines. The expression level of KLF8 is much higher in gastric cancer cells than that in normal cell via Western blot analysis. The decreased expression level of KLF8 after repression was confirmed by real-time PCR and Western blot in SGC-7901, a gastric cancer cell line. The effects of KLF8 deletion on cell proliferation and cell cycle were analyzed by MTT assay and flow cytometry, respectively. Finally, the effects of KLF8 deletion on cell apoptosis and invasion of gastric cancer cells were analyzed by Annexin staining and transwell assay, respectively. It was observed that knockdown of KLF8 reduced the cellular proliferation of SGC-7901 gastric cancer cells, a phenotype at least partially due to cell cycle arrest at G1 phase and increased apoptosis. Furthermore, the inhibition of KLF8 reduces the invasion rates of the cancer cells. Therefore, KLF8 is necessary for cell survival and invasion in gastric cancer cells. The absence of KLF8 may lead to cancer cell death. These results demonstrated that the lentivirus mediated targeted disruption of KLF8 would be an promising therapeutic method for treatment of gastric cancer.
    No preview · Article · Jul 2012 · Molecular Biology Reports
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    ABSTRACT: The Eph family of receptor tyrosine kinases has emerged as one of the pivotal regulators of tumor angiogenesis. EphA1, the first identified member of the Eph receptor family, has been found to be overexpressed in several types of human tumors. A recent report indicated that EphA1 was overexpressed in hepatocellular carcinoma (HCC) and that elevated expression of EphA1 can promote proliferation of HCC cells through stimulation by exogenous Ephrin-A1. To investigate the role of EphA1 in angiogenesis and progression of HCC, we down-regulated EphA1 by RNA interference (RNAi) technology, in an HCC-derived cell line with a high level of EphA1 expression. We established a stable knockdown clone named SiEphA1/Huh-7. The knockdown resulted in decreased proliferation of Huh-7 cells, as well as decreased motility and invasion capability in vitro. siRNA-based EphA1 knockdown also down-regulated the expression of vascular endothelial growth factor (VEGF) and matrix metalloproteinase (MMP)-2 and -9. Interestingly, the suppression of EphA1 expression in Huh-7 cells reduced their outgrowth when inoculated in the subcutaneous space in the flank of nude mice, presumably through angiogenesis inhibition since microvessel density was found to be inhibited.
    No preview · Article · Feb 2010 · Oncology Reports

Publication Stats

32 Citations
6.46 Total Impact Points


  • 2013
    • Wenzhou University
      Yung-chia, Zhejiang Sheng, China
  • 2010-2012
    • Wenzhou Medical College
      Yung-chia, Zhejiang Sheng, China