Literature DB >> 10862198

Disruption of TGFbeta signaling pathways in human pancreatic cancer cells.

D M Simeone1, T Pham, C D Logsdon.   

Abstract

OBJECTIVE: To investigate whether transforming growth factor beta (TGFbeta) signaling is disrupted in human pancreatic cancer cells, and to study the role of TGFbeta receptors and Smad genes. SUMMARY BACKGROUND DATA: TGFbeta is a known inhibitor of pancreatic growth. Disruption of the TGFbeta signaling pathway may play a role in pancreatic cancer development.
METHODS: The effect of TGFbeta on the BxPC-3, MiaPaCa-2, and PANC-1 pancreatic cancer cell lines was evaluated by [3H]thymidine incorporation and a TGFbeta-responsive reporter assay. Expression of TGFbeta receptors and Smads 2 and 3 was assessed by cross-linking assays and reverse transcriptase-polymerase chain reaction (RT-PCR). The ability to restore TGFbeta responsiveness was evaluated by transfection of TGFbeta signaling components.
RESULTS: TGFbeta produced little inhibition of DNA synthesis and did not activate a TGFbeta-responsive reporter in pancreatic cancer cell lines. 125TGFbeta cross-linking and RT-PCR confirmed the presence of TGFbeta receptors and Smad2 and Smad3 transcripts. Transfection of TGFbeta receptors or Smads 2 and 3 did not restore responsiveness. However, transfection of Smad4 into the BxPC-3 pancreatic cancer cell line restored TGFbeta responsiveness.
CONCLUSIONS: Pancreatic cancer cells show loss of TGFbeta responsiveness. Smads 2 and 3 and TGFbeta receptors are not defective in the cell lines studied. Transfection of Smad4 into one of the cell lines restored TGFbeta responsiveness, suggesting an important role for Smad4 in pancreatic cancer. It is likely that other, as yet unidentified genes are important in TGFbeta resistance in pancreatic cancer cells.

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Year:  2000        PMID: 10862198      PMCID: PMC1421110          DOI: 10.1097/00000658-200007000-00011

Source DB:  PubMed          Journal:  Ann Surg        ISSN: 0003-4932            Impact factor:   12.969


  35 in total

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