VEGF receptor expression on reactive breast cancer stroma: paving the way for tumor invasion

Hooper, Allyssa; Akiri, Gal; Jin, Dong; Shmelkov, Sergey V.; Chuang, E; Shin, Shyi Jang; Wu, Yiping; Hicklin, Dan; Rafii, Soumaya; Vahdat, L. T.

doi:10.1200/jco.2005.23.16_suppl.9642

Cited by 3 publications

(2 citation statements)

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“…For example, NF-κB-mediated IL-6 promotes cancer cell proliferation and invasion [29] . We examined the cytokines secreted by MDA-MB-231 cells in culture supernatants involving IL-6, TGF-β, VEGF and MMP9 which are required for cancer cellular invasion and metastasis [30] , [31] , [32] , [33] . Among the cytokines we investigated, IL-6 and TGF-β increased up to 5-folds and 7-folds respectively after TLR2 stimulation with PGN-SA ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Accumulated evidences showed that the consequence of NF-κB signaling associated with cytokine secretion and cytokines secreted by cancer cells exerted an important effect on control of cancer cell biology such as proliferation, EMT and invasion [42] . For examples, IL-6 promotes cancer cell proliferation and recent studies showed that IL-6 also contributed to cancer cell malignant properties and effusion respectively in lung and breast cancer [43] , [44] ; TGF-β induces cancer cell invasion and EMT in breast cancer [27] , [45] ; VEGF and MMP9 are also regarded as indispensable cytokines for breast cancer cell invasion, adhesion and metastasis [32] , [46] . We indicated that PGN-SA challenged cancer cells produce more amounts of these cytokines contributing MDA-MB-231 cells to be more invasive and adhesive.…”

Section: Discussionmentioning

confidence: 99%

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Bacteria Peptidoglycan Promoted Breast Cancer Cell Invasiveness and Adhesiveness by Targeting Toll-Like Receptor 2 in the Cancer Cells

Xie¹,

Huang²,

Xie³

et al. 2010

PLoS ONE

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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 IκB in the TLR2-NF-κB pathway of the cancer cells and stimulated IL-6 and TGF-β secretion in MDA-MB-231 cells. All these effects were abrogated by TLR2 blockade. Further investigation showed that the NF-κB, STAT3 and Smad3 activities were augmented sequentially in MDA-MB-231 cells after PGN-SA stimulation. Phosphorylation of NF-κBp65 was initially increased and then followed by phosphorylation of STAT3 and Smad3 in the delayed 4 or 6 hours. NF-κB 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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