Down-regulation of STAT3 expression by vector-based small interfering RNA inhibits pancreatic cancer growth

World J Gastroenterol. 2011 Jul 7;17(25):2992-3001. doi: 10.3748/wjg.v17.i25.2992.


Aim: To evaluate the effect of RNA interference (RNAi) mediated silence of signal transduction and activation of transcription (STAT)3 on the growth of human pancreatic cancer cells both in vitro and in vivo.

Methods: STAT3 specific shRNA was used to silence the expression of STAT3 in pancreatic cancer cell line SW1990. The anti-growth effects of RNAi against STAT3 were studied in vitro and in experimental cancer xenografts in nude mice. The potential pathways involved in STAT3 signaling were detected using reverse transcription polymerase chain reaction and western blotting.

Results: The expression of the STAT3 was inhibited using RNAi in SW1990 cells. RNAi against STAT3 inhibited cell proliferation, induced cell apoptosis and significantly reduced the levels of CyclinD1 and Bcl-xL when compared with parental and control vector-transfected cells. In vivo experiments showed that RNAi against STAT3 inhibited the tumorigenicity of SW1990 cells and significantly suppressed tumor growth when it was directly injected into tumors.

Conclusion: STAT3 signaling pathway plays an important role in the progression of pancreatic cancer, and silence of STAT3 gene using RNAi technique may be a novel therapeutic option for treatment of pancreatic cancer.

Keywords: Growth; Pancreatic cancer; RNA interference; Signal transduction and activation of transcription 3.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Cell Line, Tumor
  • Cell Proliferation
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic
  • Genetic Vectors / genetics*
  • Genetic Vectors / metabolism
  • Humans
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Neoplasm Transplantation
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / pathology*
  • RNA, Small Interfering / genetics
  • RNA, Small Interfering / metabolism*
  • STAT3 Transcription Factor / genetics
  • STAT3 Transcription Factor / metabolism*
  • Signal Transduction / physiology
  • bcl-X Protein / genetics
  • bcl-X Protein / metabolism


  • Bcl2l1 protein, mouse
  • Ccnd1 protein, mouse
  • RNA, Small Interfering
  • STAT3 Transcription Factor
  • bcl-X Protein
  • Cyclin D1