Linked Life Data

17721085

Source:http://linkedlifedata.com/resource/pubmed/id/17721085

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
16
pubmed:dateCreated
2007-8-29
pubmed:abstractText
Human papillomaviruses (HPVs) could be important risk factors for breast carcinogenesis and metastasis, as roughly 50% of breast cancers are positive for high-risk HPVs. To determine the role of high-risk HPVs in human breast carcinogenesis and metastasis, we examined the effect of E6/E7 of HPV type 16 in two non-invasive breast cancer cell lines, MCF7 and BT20. We report that E6/E7 of HPV type 16 induces cell invasive and metastatic abilities of MCF7 and BT20 in vitro and in vivo, respectively, in comparison with the wild type cells. This is accompanied by an upregulation of Id-1, a family member of helix-loop-helix (HLH) transcription factors, in MCF7 and BT20 cell lines which express E6/E7. Earlier studies have reported that Id-1 regulates cell invasion and metastasis of human breast cancer cells. To gauge the role of Id-1 in cell invasion and metastasis induced by E6/E7 of HPV type 16, we investigated the effect of E6/E7 in mouse normal embryonic fibroblast (NEF) and knockout Id-1 (Id-1(-/-)) cells. We establish that E6/E7 induces cell invasive ability in NEF but not Id-1(-/-) cells; moreover, we were able to inhibit the invasion ability of MCF7-E6/E7 and BT20-E6/E7 using Id-1 antisense retroviruses. Furthermore, we report that E6/E7 oncoproteins up-regulate Id-1 promoter activity in MCF7 and BT20 cells. We also found that HPV type 16 is present in all invasive and metastatic breast cancer and less frequently in in-situ breast cancer as opposed to normal mammary tissue. In parallel, we demonstrate that Id-1 overexpression is correlated with the presence of HPV type 16 in human invasive and metastatic breast cancer. These data suggest that high-risk HPV infections can induce cell invasion and metastasis in breast cancer through Id-1 regulation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1551-4005
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2038-42
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17721085-Animals, pubmed-meshheading:17721085-Breast Neoplasms, pubmed-meshheading:17721085-Cell Line, Tumor, pubmed-meshheading:17721085-Cell Transformation, Neoplastic, pubmed-meshheading:17721085-Cells, Cultured, pubmed-meshheading:17721085-Female, pubmed-meshheading:17721085-Humans, pubmed-meshheading:17721085-Inhibitor of Differentiation Protein 1, pubmed-meshheading:17721085-Lung Neoplasms, pubmed-meshheading:17721085-Mammary Neoplasms, Experimental, pubmed-meshheading:17721085-Mice, pubmed-meshheading:17721085-Mice, Nude, pubmed-meshheading:17721085-Mutation, pubmed-meshheading:17721085-Neoplasm Invasiveness, pubmed-meshheading:17721085-Oncogene Proteins, Viral, pubmed-meshheading:17721085-Papillomavirus E7 Proteins, pubmed-meshheading:17721085-Repressor Proteins, pubmed-meshheading:17721085-Transfection, pubmed-meshheading:17721085-Transplantation, Heterologous
pubmed:year
2007
pubmed:articleTitle
E6/E7 of HPV type 16 promotes cell invasion and metastasis of human breast cancer cells.
pubmed:affiliation
Program in Cancer Genetics, Oncology Department, McGill University, Montreal, Quebec, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't