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Fig. 1 | Breast Cancer Research

Fig. 1

From: Acquisition of epithelial-mesenchymal transition phenotype in the tamoxifen-resistant breast cancer cell: a new role for G protein-coupled estrogen receptor in mediating tamoxifen resistance through cancer-associated fibroblast-derived fibronectin and β1-integrin signaling pathway in tumor cells

Fig. 1

Immunohistochemical staining of β1-integrin, G protein-coupled estrogen receptor (GPER) and epithelial-mesenchymal transition (EMT) marker proteins in breast cancer tissues. The predominant staining pattern of GPER, vimentin and fibronectin was cytoplasmic in carcinoma tissues, whereas β1-integrin and E-cadherin were expressed mainly on the plasma membrane (A). (a-d) β1-integrin immunostaining showing representative negative (a), weak (b), moderate (c) or strong positive plasma membrane staining (d). (e-h) GPER staining showing representative negative (e), weak (f), moderate (g) or strong positive staining (h). (i-n) EMT marker proteins staining showing representative weak staining ((i) E-cadherin (k) vimentin (m) fibronectin) and strong staining ((j) E-cadherin (l) vimentin (n) fibronectin). (o,p) Example of weak β1-integrin staining in primary tumor (PT) (o) and strong β1-integrin expression in the corresponding metastasis (MT) (p) under tamoxifen treatment. Original magnification ×400. Matched change (B) and quantitative (C) comparison of β1-integrin expression in PTs and their corresponding MTs. The correlation of β1-integrin and GPER expression in MTs revealed through pair-wise scatter plots (D)

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