Knockdown of ZFR suppresses cell proliferation and invasion of human pancreatic cancer

• Xiaolan Zhao ^[3] ; Man Chen ^[1] ; Jishan Tan ^[2]
  1. [1] Chengdu Medical College

     Chengdu Medical College

     China

     
  2. [2] Chengdu Military General Hospital

     Chengdu Military General Hospital

     China

     
  3. [3] Medical Universit Hospital of Third Military Medical University Health Management Center

  Mostrar afiliaciones +
• Localización: Biological Research, ISSN-e 0717-6287, ISSN 0716-9760, Nº. 49, 2016, 8 págs.
• Idioma: inglés
• Enlaces
  • Texto completo
• Resumen

  • Zinc finger RNA binding protein (ZFR) is involved in the regulation of growth and cancer development. However, little is known about ZFR function in pancreatic cancer. Methods: Herein, to investigate whether ZFR is involved in tumor growth, Oncomine microarray data was firstly used to evaluate ZFR gene expression in human pancreatic tumors. Then short hairpin RNA (shRNA) targeting ZFR was designed and delivered into PANC-1 pancreatic cancer cells to knock down ZFR expression. Cell viability, cell proliferation and cell cycle analysis after ZFR knockdown were determined by MTT, colony forming and FACS, respectively. In addition, cell migration and invasion were assessed using the Transwell system. RESULTS: The expression of ZFR was significantly higher in pancreatic tumors than normal pancreas tissues by Oncomine database analysis. Knockdown of ZFR by shRNA-expressing lentivirus significantly decreased the viability and invasion ability of pancreatic cancer cells. Moreover, FACS analysis showed that knockdown of ZFR in PANC-1 cells caused a significant cell cycle arrest at G0/G1 phase. Furthermore, knockdown of ZFR decreased the levels of CDK2, CDK4, CyclinA and CyclinD1 and enhanced the expression of p27, which has evidenced by qRT-PCR and Western blot analysis. Conclusions: Knockdown of ZFR might provide a novel alternative to targeted therapy of pancreatic cancer and deserves further investigation.