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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2010-6-3
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pubmed:abstractText |
Chronic bacterial infection increased the risk of many solid malignancies and the underlying mechanism is usually ascribed to bacterial-caused inflammation. However, the direct interaction of infectious bacteria with cancer cells has been largely overlooked. We identified that highly metastatic breast cancer MDA-MB-231 cells expressed high level of Toll-like receptor 2 (TLR2) in contrast to poorly metastatic breast cancer cells and homogenous untransformed breast cells. TLR2 in MDA-MB-231 cells were actively triggered by peptidoglycan (PGN) from infectious bacterium Staphylococcus aureus (PGN-SA), resulting in the promoted invasiveness and adhesiveness of the cancer cells in vitro. PGN-SA induced phosphorylation of TAK1 and IkappaB in the TLR2-NF-kappaB pathway of the cancer cells and stimulated IL-6 and TGF-beta secretion in MDA-MB-231 cells. All these effects were abrogated by TLR2 blockade. Further investigation showed that the NF-kappaB, STAT3 and Smad3 activities were augmented sequentially in MDA-MB-231 cells after PGN-SA stimulation. Phosphorylation of NF-kappaBp65 was initially increased and then followed by phosphorylation of STAT3 and Smad3 in the delayed 4 or 6 hours. NF-kappaB inhibition attenuated STAT3 and Smad3 activities whereas PGN-SA-stimulated cell culture supernatants reversed these inhibitory effects. Our study indicated that TLR2 activation by infectious bacterial PGN played an important role in breast cancer cell invasiveness and illustrated a new link between infectious bacteria and the cancer cells, suggesting the importance of antibiotic therapy to treat cancer with bacterial infection.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-11464285,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-11725828,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-12000178,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-12490959,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-14505311,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-15170447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-15314694,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-15585605,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-15655344,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-15829287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16103425,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16244651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16496371,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16514135,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16518408,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16585585,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16603636,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16724054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16849519,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-16912176,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17032697,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17038530,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17043764,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17159986,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17186030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17192546,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17198080,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17261761,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17373717,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17476347,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17479101,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17483348,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17505005,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17908958,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17952090,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-17974996,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18006895,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18060028,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18060036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18337322,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18796565,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20520770-18840819
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidoglycan,
http://linkedlifedata.com/resource/pubmed/chemical/SMAD3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Smad3 Protein,
http://linkedlifedata.com/resource/pubmed/chemical/TLR2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:issn |
1932-6203
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
e10850
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pubmed:dateRevised |
2010-9-28
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pubmed:meshHeading |
pubmed-meshheading:20520770-Breast Neoplasms,
pubmed-meshheading:20520770-Cell Adhesion,
pubmed-meshheading:20520770-Cell Line, Tumor,
pubmed-meshheading:20520770-Female,
pubmed-meshheading:20520770-Gene Expression Profiling,
pubmed-meshheading:20520770-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:20520770-Humans,
pubmed-meshheading:20520770-Interleukin-6,
pubmed-meshheading:20520770-NF-kappa B,
pubmed-meshheading:20520770-Neoplasm Invasiveness,
pubmed-meshheading:20520770-Peptidoglycan,
pubmed-meshheading:20520770-STAT3 Transcription Factor,
pubmed-meshheading:20520770-Signal Transduction,
pubmed-meshheading:20520770-Smad3 Protein,
pubmed-meshheading:20520770-Staphylococcus aureus,
pubmed-meshheading:20520770-Toll-Like Receptor 2,
pubmed-meshheading:20520770-Transforming Growth Factor beta
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pubmed:year |
2010
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pubmed:articleTitle |
Bacteria peptidoglycan promoted breast cancer cell invasiveness and adhesiveness by targeting toll-like receptor 2 in the cancer cells.
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pubmed:affiliation |
Biology Research Institute of the United Laboratories International Holdings Limited, Zhuhai, China. xiewj75@126.com
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