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month download article/chapter de kier joff� tamoxifen-resistant breast cancer tamoxifen-resistant breast carcinomas matrix metalloproteinase-1-dependent invasion tamoxifen-induced cell death small-cell lung cancer soluble stromal factors spontaneous estrogen dependent mapk/erk inhibitor pd98059 mammary epithelial cells tumor microenvironment stromal-epithelial interactions blocking β1 integrin soluble factors produced pi3k/akt inhibitor ly294002 epithelial tumor cells breast cancer cells estrogen receptor alpha full article pdf marina simian growth factor signalling human breast cancer advanced breast cancer breast cancer prognosis invasive breast cancer protects tumor cells breast tumor fibroblasts suggesting stromal factors modulate tamoxifen resistance mesenchymal conversion increased beta1 integrin privacy choices/manage cookies breast cancer progression related subjects gutierrez mc stromal cellular responses de-ac02-05ch1123 integrin fibronectin receptors understand estrogen responsiveness endocrine-sensitive cells health effects division epithelial cell morphology β1 integrin mapk/erk 1/2 pathways gene expression profiling confers endocrine resistance article pontiggia selective estrogen modulators extracellular matrix regulation

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         headline:The tumor microenvironment modulates tamoxifen resistance in breast cancer: a role for soluble stromal factors and fibronectin through β1 integrin
         description:Tamoxifen resistance has been largely attributed to genetic alterations in the epithelial tumor cells themselves, such as overexpression of HER-2/Neu. However, in the clinic, only about 15–20% of cases of HER-2/Neu amplification has actually been correlated to the acquisition of endocrine resistance, suggesting that other mechanisms must be involved as well. Using the epithelial LM05-E and the fibroblastic LM05-F cell lines, derived from the estrogen dependent spontaneous M05 mouse mammary tumor, as well as MCF-7 cells, we analyzed whether soluble stromal factors or extracellular matrix components protected against tamoxifen induced cell death. Involvement of signaling pathways was determined by using specific inhibitors and western blot, and phosphorylation of the estrogen receptor alpha by western blot and immunofluorescence. Soluble factors produced by the fibroblastic cells protect the epithelial tumor cells from tamoxifen-induced cell death through a mechanism that involves EGFR and matrix metalloproteinases upstream of PI3K/AKT. Exogenous fibronectin by itself confers endocrine resistance through interaction with β1 integrin and activation of PI3K/AKT and MAPK/ERK 1/2 pathways. The conferred resistance is reversed by blocking β1 integrin. We show also that treatment with both conditioned medium and fibronectin leads to the phosphorylation of the estrogen receptor at serine-118, suggesting stromal factors as modulators of ER activity. Our results show that the tumor microenvironment can modulate tamoxifen resistance, providing an alternative explanation for why patients become refractory to hormone-therapy.
         datePublished:2011-09-21T00:00:00Z
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            Tamoxifen resistance
            Estrogen receptor
            Tumor microenvironment
            Fibronectin
            Soluble stromal factors
            β1 integrin
            Oncology
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      headline:The tumor microenvironment modulates tamoxifen resistance in breast cancer: a role for soluble stromal factors and fibronectin through β1 integrin
      description:Tamoxifen resistance has been largely attributed to genetic alterations in the epithelial tumor cells themselves, such as overexpression of HER-2/Neu. However, in the clinic, only about 15–20% of cases of HER-2/Neu amplification has actually been correlated to the acquisition of endocrine resistance, suggesting that other mechanisms must be involved as well. Using the epithelial LM05-E and the fibroblastic LM05-F cell lines, derived from the estrogen dependent spontaneous M05 mouse mammary tumor, as well as MCF-7 cells, we analyzed whether soluble stromal factors or extracellular matrix components protected against tamoxifen induced cell death. Involvement of signaling pathways was determined by using specific inhibitors and western blot, and phosphorylation of the estrogen receptor alpha by western blot and immunofluorescence. Soluble factors produced by the fibroblastic cells protect the epithelial tumor cells from tamoxifen-induced cell death through a mechanism that involves EGFR and matrix metalloproteinases upstream of PI3K/AKT. Exogenous fibronectin by itself confers endocrine resistance through interaction with β1 integrin and activation of PI3K/AKT and MAPK/ERK 1/2 pathways. The conferred resistance is reversed by blocking β1 integrin. We show also that treatment with both conditioned medium and fibronectin leads to the phosphorylation of the estrogen receptor at serine-118, suggesting stromal factors as modulators of ER activity. Our results show that the tumor microenvironment can modulate tamoxifen resistance, providing an alternative explanation for why patients become refractory to hormone-therapy.
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         Breast cancer
         Tamoxifen resistance
         Estrogen receptor
         Tumor microenvironment
         Fibronectin
         Soluble stromal factors
         β1 integrin
         Oncology
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