scholarly journals Steroid receptor coactivator 3 regulates autophagy in breast cancer cells through macrophage migration inhibitory factor

Cell Research ◽  
2012 ◽  
Vol 22 (6) ◽  
pp. 1003-1021 ◽  
Author(s):  
Mei-Yi Wu ◽  
Junjiang Fu ◽  
Jianming Xu ◽  
Bert W O'Malley ◽  
Ray-Chang Wu
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Breast Cancer Cells ◽  
Steroid Receptor ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Steroid Receptor Coactivator

scholarly journals miR-451a Inhibited Cell Proliferation and Enhanced Tamoxifen Sensitive in Breast Cancer via Macrophage Migration Inhibitory Factor

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Zhenru Liu ◽  
Tianyu Miao ◽  
Ting Feng ◽  
Zhouhua Jiang ◽  
Mingyuan Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Migration Inhibitory Factor ◽  
Colony Formation ◽  
Macrophage Migration Inhibitory Factor ◽  
Breast Cancer Cells ◽  
Lentiviral Vectors ◽  
Inhibitory Factor ◽  
Macrophage Migration

This study aims to investigate the regulative effects of microRNA-451a (miR-451a) on cell proliferation and sensitivity to tamoxifen in breast cancer cells. In cell culture experiments, the lentiviral vectors of pHBLV-miR-451a and pHBLV-miR-451a sponge were constructed and used to transfect MCF-7 and LCC2 cells. The transfection efficiency was tested by fluorescent observation, and cell lines with stable over- or downregulated expression of miR-451a were established. The expression of miR-451a and the target gene macrophage migration inhibitory factor (MIF) were detected by real-time reverse transcriptase polymerase chain reaction and/or western blot. Moreover, MTT assay, colony formation, and Transwell invasion assays were also performed. Data showed that the recombinant lentiviral vectors were constructed correctly, and the virus titer was 1 × 108 CFU/mL. The stable transfected cells were obtained. Overexpression of miR-451a downregulated MIF expression in mRNA and protein levels and inhibited cell proliferation, colony formation, and invasion of breast cancer cells. Downregulation of miR-451a upregulated MIF expression and increased breast cancer cell growth, invasion, and tamoxifen sensitivity. In summary, the miR-451a/MIF pathway may play important roles in the biological properties of breast cancer cells and may be a potential therapeutic target for breast cancer.

scholarly journals Autophagy Inhibition Induces the Secretion of Macrophage Migration Inhibitory Factor (MIF) with Autocrine and Paracrine Effects on the Promotion of Malignancy in Breast Cancer

Biology ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 20 ◽  
Author(s):  
Israel Cotzomi-Ortega ◽  
Arely Rosas-Cruz ◽  
Dalia Ramírez-Ramírez ◽  
Julio Reyes-Leyva ◽  
Miriam Rodriguez-Sosa ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Migration Inhibitory Factor ◽  
Macrophage Migration Inhibitory Factor ◽  
Cell Types ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Breast Cancers ◽  
Paracrine Effects ◽  
Autophagy Inhibition

Breast cancer is the main cause of cancer-related death in women in the world. Because autophagy is a known survival pathway for cancer cells, its inhibition is currently being explored in clinical trials for treating several types of malignancies. In breast cancer, autophagy has been shown to be necessary for the survival of cancer cells from the triple negative subtype (TNBC), which has the worst prognosis among breast cancers and currently has limited therapeutic options. Autophagy has also been involved in the regulation of protein secretion and, of importance for this work, the inhibition of autophagy is known to promote the secretion of proinflammatory cytokines from distinct cell types. We found that the inhibition of autophagy in TNBC cell lines induced the secretion of the macrophage migration inhibitory factor (MIF), a pro-tumorigenic cytokine involved in breast cancer invasion and immunomodulation. MIF secretion was dependent on an increase in reactive oxygen species (ROS) induced by the inhibition of autophagy. Importantly, MIF secreted from autophagy-deficient cells increased the migration of cells not treated with autophagy inhibitors, indicating that autophagy inhibition in cancer cells promoted malignancy in neighboring cells through the release of secreted factors, and that a combinatorial approach should be evaluated for cancer therapy.

scholarly journals Dual role of macrophage migration inhibitory factor (MIF) in human breast cancer

BMC Cancer ◽  
2009 ◽  
Vol 9 (1) ◽  
Author(s):  
Eva Verjans ◽  
Erik Noetzel ◽  
Nuran Bektas ◽  
Anke K Schütz ◽  
Hongqi Lue ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Migration Inhibitory Factor ◽  
Human Breast Cancer ◽  
Macrophage Migration Inhibitory Factor ◽  
Dual Role ◽  
Inhibitory Factor ◽  
Macrophage Migration ◽  
Human Breast
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