scholarly journals Differential Response of Non-cancerous and Malignant Breast Cancer Cells to Conditioned Medium of Adipose tissue-derived Stromal Cells (ASCs)

2019 ◽  
Vol 16 (6) ◽  
pp. 893-901
Author(s):  
Yi-Chia Wu ◽  
Wei-Ting Wang ◽  
Li-Ju Huang ◽  
Ruo-You Cheng ◽  
Yur-Ren Kuo ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Stromal Cells ◽  
Breast Cancer Cells ◽  
Differential Response ◽  
Malignant Breast

scholarly journals Epinephrine Infiltration of Adipose Tissue Impacts MCF7 Breast Cancer Cells and Total Lipid Content

2019 ◽  
Vol 20 (22) ◽  
pp. 5626 ◽  
Author(s):  
Pierre Avril ◽  
Luciano Vidal ◽  
Sophie Barille-Nion ◽  
Louis-Romée Le Nail ◽  
Françoise Redini ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Tumor Progression ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Lipid Composition ◽  
Breast Cancer Cells ◽  
Quiescent State ◽  
Mcf7 Cells ◽  
Mesenchymal Transition

Background: Considering the positive or negative potential effects of adipocytes, depending on their lipid composition, on breast tumor progression, it is important to evaluate whether adipose tissue (AT) harvesting procedures, including epinephrine infiltration, may influence breast cancer progression. Methods: Culture medium conditioned with epinephrine-infiltrated adipose tissue was tested on human Michigan Cancer Foundation-7 (MCF7) breast cancer cells, cultured in monolayer or in oncospheres. Lipid composition was evaluated depending on epinephrine-infiltration for five patients. Epinephrine-infiltrated adipose tissue (EI-AT) or corresponding conditioned medium (EI-CM) were injected into orthotopic breast carcinoma induced in athymic mouse. Results: EI-CM significantly increased the proliferation rate of MCF7 cells Moreover EI-CM induced an output of the quiescent state of MCF7 cells, but it could be either an activator or inhibitor of the epithelial mesenchymal transition as indicated by gene expression changes. EI-CM presented a significantly higher lipid total weight compared with the conditioned medium obtained from non-infiltrated-AT of paired-patients. In vivo, neither the EI-CM or EI-AT injection significantly promoted MCF7-induced tumor growth. Conclusions: Even though conditioned media are widely used to mimic the secretome of cells or tissues, they may produce different effects on tumor progression, which may explain some of the discrepancy observed between in vitro, preclinical and clinical data using AT samples.

Interaction of human adipose tissue-derived mesenchymal stromal cells with breast cancer cells

Neoplasma ◽  
2011 ◽  
Vol 58 (5) ◽  
pp. 361-370 ◽  
Author(s):  
L. KUCEROVA ◽  
M. KOVACOVICOVA ◽  
S. POLAK ◽  
M. BOHAC ◽  
J. FEDELES ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Adipose Tissue ◽  
Cancer Cells ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Breast Cancer Cells ◽  
Human Adipose Tissue

A novel 3-D bio-microfluidic system mimicking in vivo heterogeneous tumour microstructures reveals complex tumour–stroma interactions

Lab on a Chip ◽  
2017 ◽  
Vol 17 (16) ◽  
pp. 2852-2860 ◽  
Author(s):  
Qihui Fan ◽  
Ruchuan Liu ◽  
Yang Jiao ◽  
Chunxiu Tian ◽  
James D. Farrell ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Invasive Breast Cancer ◽  
Stromal Cells ◽  
Breast Cancer Cells ◽  
Microfluidic System ◽  
Tumour Stroma ◽  
Collagen Hydrogel

A 3-D microfluidic system consisting of microchamber arrays embedded in a collagen hydrogel with tunable biochemical gradients was constructed for investigating interactions between invasive breast cancer cells and stromal cells.

scholarly journals The effect of adipocyte–macrophage crosstalk in obesity-related breast cancer

2019 ◽  
Vol 62 (3) ◽  
pp. R201-R222 ◽  
Author(s):  
Ayse Basak Engin ◽  
Atilla Engin ◽  
Ipek Isik Gonul
Keyword(s):  
Breast Cancer ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Cancer Cells ◽  
Inflammatory Cytokines ◽  
Breast Cancer Cells ◽  
Sirtuin 1 ◽  
Aromatase Activity ◽  
Breast Adipose Tissue ◽  
Mtorc1 Signaling

Adipose tissue is the primary source of many pro-inflammatory cytokines in obesity. Macrophage numbers and pro-inflammatory gene expression are positively associated with adipocyte size. Free fatty acid and tumor necrosis factor-α involve in a vicious cycle between adipocytes and macrophages aggravating inflammatory changes. Thereby, M1 macrophages form a characteristic ‘crown-like structure (CLS)’ around necrotic adipocytes in obese adipose tissue. In obese women, CLSs of breast adipose tissue are responsible for both increase in local aromatase activity and aggressive behavior of breast cancer cells. Interlinked molecular mechanisms between adipocyte–macrophage–breast cancer cells in obesity involve seven consecutive processes: Excessive release of adipocyte- and macrophage-derived inflammatory cytokines, TSC1–TSC2 complex–mTOR crosstalk, insulin resistance, endoplasmic reticulum (ER) stress and excessive oxidative stress generation, uncoupled respiration and hypoxia, SIRT1 controversy, the increased levels of aromatase activity and estrogen production. Considering elevated risks of estrogen receptor (E2R)-positive postmenopausal breast cancer growth in obesity, adipocyte–macrophage crosstalk is important in the aforementioned issues. Increased mTORC1 signaling in obesity ensures the strong activation of oncogenic signaling in E2Rα-positive breast cancer cells. Since insulin and insulin-like growth factors have been identified as tumor promoters, hyperinsulinemia is an independent risk factor for poor prognosis in breast cancer despite peripheral insulin resistance. The unpredictable effects of adipocyte-derived leptin–estrogen–macrophage axis, and sirtuin 1 (SIRT1)–adipose-resident macrophage axis in obese postmenopausal patients with breast cancer are unresolved mechanistic gaps in the molecular links between the tumor growth and adipocytokines.

scholarly journals Interleukin 6 secreted from adipose stromal cells promotes migration and invasion of breast cancer cells

Oncogene ◽  
2009 ◽  
Vol 28 (30) ◽  
pp. 2745-2755 ◽  
Author(s):  
M Walter ◽  
S Liang ◽  
S Ghosh ◽  
P J Hornsby ◽  
R Li
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Stromal Cells ◽  
Interleukin 6 ◽  
Breast Cancer Cells ◽  
Migration And Invasion ◽  
Adipose Stromal Cells

scholarly journals Osteoblast-conditioned medium promotes proliferation and sensitizes breast cancer cells to imatinib treatment

2007 ◽  
Vol 14 (1) ◽  
pp. 61-72 ◽  
Author(s):  
Marina Brama ◽  
Sabrina Basciani ◽  
Sara Cherubini ◽  
Stefania Mariani ◽  
Silvia Migliaccio ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Tyrosine Kinase ◽  
Cancer Cells ◽  
Conditioned Medium ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Imatinib Treatment ◽  
Human Breast ◽  
Mcf 7

Inhibition of platelet-derived growth factor receptor (PDGFR) signaling restricts the growth of human breast cancer in the bone of nude mice. We hypothesized that osteoblast-secreted substances may alter the response capacity of breast cancer cells to the PDGFRs tyrosine kinase inhibitor imatinib mesylate. We found that osteoblast-conditioned medium (OCM) increases the proliferation rate of the estrogen receptor negative (ER−) MDA-MB-231 and of the ER+ MCF-7 human breast cancer cell lines and the growth-promoting effect on ER+ cells is independent from estrogen. OCM significantly improved the dose- and the time-dependent sensitivity of the tumor cells to the anti-proliferative effect of imatinib. We also found that MDA-MB-231 and MCF-7 cells express the two PDGFRs subtypes, PDGFR-α and PDGFR-β, and OCM treatment increases the expression of the PDGFRs. Furthermore, imatinib inhibited the phosphorylation rate of its target tyrosine kinase receptors. We conclude that bone microenvironment, through osteoblast-secreted substances may cause estrogen-independent proliferation of breast cancer cells by a mechanism mediated by the induction of PDGFRs expression. The enhanced sensitivity of OCM-treated breast cancer cells to imatinib would justify investigation on the efficacy of imatinib in bone breast cancer metastasis.

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