Phenotype and genotype of pancreatic cancer cell lines - PubMed (original) (raw)

Review

Phenotype and genotype of pancreatic cancer cell lines

Emily L Deer et al. Pancreas. 2010 May.

Erratum in

Abstract

The dismal prognosis of pancreatic adenocarcinoma is due in part to a lack of molecular information regarding disease development. Established cell lines remain a useful tool for investigating these molecular events. Here we present a review of available information on commonly used pancreatic adenocarcinoma cell lines as a resource to help investigators select the cell lines most appropriate for their particular research needs. Information on clinical history; in vitro and in vivo growth characteristics; phenotypic characteristics, such as adhesion, invasion, migration, and tumorigenesis; and genotypic status of commonly altered genes (KRAS, p53, p16, and SMAD4) was evaluated. Identification of both consensus and discrepant information in the literature suggests careful evaluation before selection of cell lines and attention be given to cell line authentication.

PubMed Disclaimer

Figures

Figure 1

Figure 1

Relative expression of COX-2 in PA cell lines. Basal expression of COX-2 was determined by Western blot analysis in PA cell line lysates and quantified by densitometry. A: Representative Western blot. All cell lines were acquired from the American Type Culture Collection (ATCC, Manassas, VA) and propagated in ATCC recommended media. Cells were grown to 80% confluence before preparation of cell lysates. Proteins were separated by SDS-polyacrylamide gel electrophoresis and transferred to PVDF membranes using standard protocols. The membranes were probed with antibodies to COX-2 (mouse monoclonal, Cayman Chemical, Ann Arbor, MI) and β-actin (rabbit monoclonal, Cell Signaling Technology, Danvers, MA) or GAPDH (mouse monoclonal, Novus Biologicals, Littleton, CO) as total protein loading controls. B: Densitometric analyses. Autoradiographs of Western blots were quantified using ImageJ software (National Institutes of Health,

http://rsb.info.nih.gov/ij/

). COX-2 intensity was first normalized to the corresponding loading control (β-actin or GAPDH) and then normalized to the BxPC-3 ratio for each blot. Data represents the combined results of four independent experiments (mean ± SEM).

Similar articles

Cited by

References

    1. Jones S, Zhang X, Parsons DW, et al. Core signaling pathways in human pancreatic cancers revealed by global genomic analyses. Science. 2008;321:1801–1806. - PMC - PubMed
    1. Douglas EJ, Fiegler H, Rowan A, et al. Array comparative genomic hybridization analysis of colorectal cancer cell lines and primary carcinomas. Cancer Res. 2004;64:4817–4825. - PubMed
    1. Larramendy ML, Lushnikova T, Bjorkqvist AM, et al. Comparative genomic hybridization reveals complex genetic changes in primary breast cancer tumors and their cell lines. Cancer Genet Cytogenet. 2000;119:132–138. - PubMed
    1. Arumugam T, Simeone DM, Van Golen K, et al. S100P promotes pancreatic cancer growth, survival, and invasion. Clin Cancer Res. 2005;11:5356–5364. - PubMed
    1. Marchesi F, Monti P, Leone BE, et al. Increased survival, proliferation, and migration in metastatic human pancreatic tumor cells expressing functional CXCR4. Cancer Res. 2004;64:8420–8427. - PubMed

Publication types

MeSH terms

Substances

LinkOut - more resources