pubmed-article:21502401 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21502401 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
pubmed-article:21502401 | lifeskim:mentions | umls-concept:C1367307 | lld:lifeskim |
pubmed-article:21502401 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:21502401 | lifeskim:mentions | umls-concept:C1148673 | lld:lifeskim |
pubmed-article:21502401 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:21502401 | pubmed:issue | 11 | lld:pubmed |
pubmed-article:21502401 | pubmed:dateCreated | 2011-6-2 | lld:pubmed |
pubmed-article:21502401 | pubmed:abstractText | Both STAT3 and NF-?B are persistently activated in diverse cancers and promote tumor cell proliferation, survival, angiogenesis, and metastasis through transcriptional activation of multiple common genes. Paradoxically, STAT3 also suppresses many NF-?B-inducible genes involved in innate and adaptive antitumor immunity in spite of elevated levels of NF-?B in tumors. In this study, we show that expression of many NF-?B downstream target genes in tumors depends on STAT3 DNA binding. When STAT3 is elevated in tumor cells and tumor-infiltrating immune cells, persistently activated NF-?B interacts with STAT3 and preferentially binds to genes with STAT3-binding site(s) in promoters. A large number of NF-?B downstream genes associated with oncogenesis and chronic inflammation contain STAT3 DNA-binding site(s). However, in contrast, many genes frequently associated with antitumor immunity lack STAT3 DNA-binding site(s) and can only be activated by NF-?B when STAT3 is inhibited in tumors. The introduction of STAT3 DNA-binding sequences by site-specific mutagenesis in an immunostimulatory gene promoter allows its transcriptional activation by NF-?B in tumor cells. Furthermore, STAT3 facilitates NF-?B binding to genes that are important for tumor growth while inhibiting its binding to Th-1 immunostimulatory genes in growing tumors, including in tumor-infiltrating immune cells. The results of this study provide insight into how some of the oncogenic/inflammatory and Th-1 immunostimulatory genes are differentially regulated in cancer. | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:language | eng | lld:pubmed |
pubmed-article:21502401 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:21502401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:21502401 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:21502401 | pubmed:month | Jun | lld:pubmed |
pubmed-article:21502401 | pubmed:issn | 1538-7445 | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:GilBB | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:LiuYongY | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:PardollDrewD | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:HongXinX | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:LeeHeehyoungH | lld:pubmed |
pubmed-article:21502401 | pubmed:author | pubmed-author:DengJiehuiJ | lld:pubmed |
pubmed-article:21502401 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:21502401 | pubmed:day | 1 | lld:pubmed |
pubmed-article:21502401 | pubmed:volume | 71 | lld:pubmed |
pubmed-article:21502401 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:21502401 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:21502401 | pubmed:pagination | 3772-80 | lld:pubmed |
pubmed-article:21502401 | pubmed:dateRevised | 2011-9-22 | lld:pubmed |
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pubmed-article:21502401 | pubmed:year | 2011 | lld:pubmed |
pubmed-article:21502401 | pubmed:articleTitle | A requirement of STAT3 DNA binding precludes Th-1 immunostimulatory gene expression by NF-?B in tumors. | lld:pubmed |
pubmed-article:21502401 | pubmed:affiliation | Department of Cancer Immunotherapeutics and Tumor Immunology, Beckman Research Institute, City of Hope National Medical Center, Duarte, California 91010, USA. | lld:pubmed |
pubmed-article:21502401 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:21502401 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
entrez-gene:6774 | entrezgene:pubmed | pubmed-article:21502401 | lld:entrezgene |
entrez-gene:20848 | entrezgene:pubmed | pubmed-article:21502401 | lld:entrezgene |
http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:21502401 | lld:entrezgene |