Linked Life Data

16707592

Source:http://linkedlifedata.com/resource/pubmed/id/16707592

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2006-5-18
pubmed:abstractText
MUC1 is a highly glycosylated, type I transmembrane protein expressed by normal ductal epithelial cells of the pancreas, breast, lung, and gastrointestinal tract, and overexpressed in many cases of adenocarcinoma. We down-regulated MUC1 expression by RNA interference and investigated the effects on malignant and metastatic potential of a human pancreatic cancer cell line, S2-013. MUC1-suppressed clones, S2-013.MTII.C1 and S2-013.MTII.C2, were established by targeting a sequence 3,151 bp from the initiation codon and characterized in vitro for proliferation, invasion, and adhesion. We evaluated the effects of MUC1 suppression in vivo on tumor growth and metastatic properties following implantation into the cecum or pancreas of athymic mice. MUC1-suppressed clones showed significantly decreased proliferation in vitro and in vivo. Global gene expression was evaluated by oligonucleotide microarray analysis. Surprisingly, genes predicted to increase doubling times (cyclin B1 and cyclin D3) were overexpressed in MUC1-suppressed clones. There were alterations in expression of several genes that may affect the malignant properties of pancreatic cancer. Adhesion of MUC1-suppressed cells in vitro to type IV collagen and fibronectin was slightly increased, and adhesion was slightly decreased to type I collagen and laminin. Results of implantation to cecum and pancreas showed significant reduction of metastasis to lymph nodes, lung, or peritoneal sites compared with S2-013.gfp-neo control cells. These results support the hypothesis that MUC1 contributes significantly to growth and metastasis, and that down-regulation of MUC1 protein expression decreases the metastatic potential of pancreatic adenocarcinoma.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
1078-0432
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2976-87
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16707592-Adenocarcinoma, pubmed-meshheading:16707592-Animals, pubmed-meshheading:16707592-Antigens, Neoplasm, pubmed-meshheading:16707592-Cell Adhesion, pubmed-meshheading:16707592-Cell Proliferation, pubmed-meshheading:16707592-Down-Regulation, pubmed-meshheading:16707592-Female, pubmed-meshheading:16707592-Gene Expression Profiling, pubmed-meshheading:16707592-Humans, pubmed-meshheading:16707592-Mice, pubmed-meshheading:16707592-Mice, Nude, pubmed-meshheading:16707592-Mucin-1, pubmed-meshheading:16707592-Mucins, pubmed-meshheading:16707592-Neoplasm Metastasis, pubmed-meshheading:16707592-Neoplasms, Experimental, pubmed-meshheading:16707592-Pancreatic Neoplasms, pubmed-meshheading:16707592-Phenotype, pubmed-meshheading:16707592-RNA, Small Interfering, pubmed-meshheading:16707592-RNA Interference, pubmed-meshheading:16707592-Tumor Cells, Cultured
pubmed:year
2006
pubmed:articleTitle
RNA interference suppression of MUC1 reduces the growth rate and metastatic phenotype of human pancreatic cancer cells.
pubmed:affiliation
Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198-6805, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural