ABSTRACT
Objective: To investigate the proliferation, adhesion, migration, invasion, and contraction capacities of carcinoma-associated fibroblasts (CAFs) in human breast cancer microenvironment. Methods: The protein expressions of fibronectin (FN), alpha-smooth-muscle actin (α-SMA) and fibroblast activation protein (FAP) were detected by Western blotting, so as to distinguish CAFs cells from normal fibroblasts (NFs). The proliferation of CAFs and NFs was detected by Roche xCellingence system, cell counting, and cell counting kit-8 (CCK-8) assay. The adhesion, migration, invasion and contraction capacities of CAFs were evaluated by the cell adhesion experiment, Roche xCellingence system, Transwell invasion assay and collagen gel contraction assay, respectively. Results: The primary CAFs and NFs cells which were isolated from human breast cancer grew in good condition with active proliferation. The linear types and trends of their growth curves were accorded with the cell growth characteristics. While compared with NFs, CAFs had a robust proliferation capacity, and the obviously stronger abilities of adhesion, migration, invasion, and contraction. Conclusion: There are prodigious differences of proliferation and migration between CAFs and NFs cells in human breast cancer microenvironment. CAFs have the stronger abilities of proliferation, adhesion, migration, invasion, and contraction than NFs. Copyright © 2013 by TUMOR.
ABSTRACT
PURPOSE: G-protein coupled estrogen receptor 1 (GPER) probably play important roles in the progression of breast cancer including endocrine therapeutic resistance. We evaluated GPER in primary breast cancers. METHODS: Immunohistochemistry was used to detect GPER in paraffin-embedded tissues of primary breast cancers from 423 patients and GPER expression was correlated with clinicopathological factors. RESULTS: GPER was expressed in 63.8% of specimens, coexpressed with estrogen receptor alpha (ERalpha) in 36.6% of tumors and was positive in 62.5% of the ERalpha-negative tumors. The expression of GPER had no relationship with the status of ERalpha, progesterone receptor and HER2. Although the expression of GPER was significantly inversely related with nodal status (p=0.045), no correlation between GPER expression and other clinicopathological variables (age, menstruation status, tumor size, stage, histologic grade, Nottingham Prognostic Index or pathological type) was found. CONCLUSION: GPER and ERalpha exhibited independent expression pattern of distribution in primary breast cancers. A long-term follow-up and a more definite molecular phenotype for ER are necessary in confirming studies.