A cystic fibrosis pancreatic adenocarcinoma cell line.

Schoumacher, Robert; Ram, Jeffrey L.; Iannuzzi, MC; Bradbury, N.A.; Wallace, Robert W.; Hon, Catherine Tom; Kelly, David R.; Schmid, Sonja; Gelder, Frank B.; Rado, Thomas A.

doi:10.1073/pnas.87.10.4012

Cited by 224 publications

(123 citation statements)

References 26 publications

(23 reference statements)

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“…The parental CFPAC1 cell line has been derived from a CF patient carrying a DF508 mutation in the CFTR (Schoumacher et al, 1990). The CFPAC1 cells were transduced with a retroviral vector (PLJ) and the CFTR-expressing viral construct (PLJ-CFTR).…”

Section: Cftr Expression Is Inversely Associated With Muc4 Expressionmentioning

confidence: 99%

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

et al. 2006

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MUC4 mucin is a high molecular weight transmembrane glycoprotein that plays important roles in tumour biology. It is aberrantly expressed in pancreatic adenocarcinoma, while not being detectable in the normal pancreas. Previous studies have demonstrated that the cystic fibrosis transmembrane conductance regulator (CFTR), a chloride channel that is defective in CF, is implicated in multiple cellular functions, including gene regulation. In the present study, using a CFTR-defective pancreatic cancer cell line and its derived subline expressing functional CFTR, we report that MUC4 expression is negatively regulated by CFTR. Short-interfering RNA (siRNA)-mediated silencing of CFTR also leads to an increased expression of MUC4. Additionally, our results suggest that CFTR-mediated regulation of MUC4 is cell densitydependent and is achieved by transcriptional and posttranslational mechanisms. Moreover, in a panel of pancreatic cancer cell lines and normal pancreas, we observed that CFTR was downregulated in pancreatic cancer cells and negatively correlated with MUC4 in most cases. An aberrant expression of MUC4 was also detected in the CF pancreas. Downregulation of CFTR in pancreatic adenocarcinoma and its inverse association with the tumour-linked mucin, MUC4, indicate novel function(s) of CFTR in pancreatic tumour biology and suggest the implication of new signalling pathway(s) in MUC4 regulation.

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Section: Cftr Expression Is Inversely Associated With Muc4 Expressionmentioning

confidence: 99%

MUC4 expression is regulated by cystic fibrosis transmembrane conductance regulator in pancreatic adenocarcinoma cells via transcriptional and post-translational mechanisms

et al. 2006

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“…Consortium CloneID 526956), which appeared to be a novel member of the cbl family, was identi®ed by a BLAST search of the National Center for Biotechnology Information (NCBI) human EST data base. This cDNA clone, derived from a cDNA library prepared from the Stratagene human pancreas adenocarcinoma cell line CFPAC-1 (Schoumacher et al, 1990), was obtained from ATCC. The 753 bp clone was sequenced and nucleotide and predicted amino comparisons revealed 60 ± 70% homology to either c-cbl (Blake et al, 1991) or cbl-b (Keane et al, 1995) over the ®rst *450 bp.…”

Section: Identi®cation and Cloning Of Cbl-3mentioning

confidence: 99%

cbl-3: a new mammalian cbl family protein

et al. 1999

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We have cloned a new human gene, cbl-3, which encodes a protein with marked homology to the cbl family of proteins. The predicted protein encoded by this gene retains the conserved phosphotyrosine binding domain (PTB) in the N-terminal and the zinc ®nger but is signi®cantly shorter (MW 52.5 kDa) than the other mammalian cbl proteins. The protein lacks the extensive proline rich domain and leucine zipper seen in c-cbl and cbl-b and structurally most resembles the C. elegans and Drosophila cbl proteins. The gene is ubiquitously expressed with highest expression in the aerodigestive tract, prostate, adrenal gland, and salivary gland. The protein is phosphorylated and recruited to the EGFR upon EGF stimulation and inhibits EGF stimulated MAP kinase activation. In comparison to the other mammalian cbl proteins (e.g. cbl-b), cbl-3 interacts with a restricted range of proteins containing Src Homology 3 regions. An alternatively spliced form of the cbl-3 protein was also identi®ed which deletes a critical region of the PTB domain and which does not interact with the EGFR nor inhibit EGF stimulated MAP kinase activation. These data demonstrate that cbl-3, a novel mammalian cbl protein, is a regulator of EGFR mediated signal transduction.

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“…PH SO0 1 4-5793(96)00900-3 carcinoma in a 40-year-old patient. CFPAC-1 is a pancreatic adenocarcinoma cell line derived from a homozygous patient for phenylalanine deletion at position 508 (AF 508) and expresses the appropriate CF gene product [18]. CFPAC-I cells were stably transfected with a retroviral vector (PLJ) that contained the full-length cDNA encoding wild type CFTR: CFPAC-PLJ-CFTR6 [19].…”

Section: Cell Linesmentioning

confidence: 99%