Hyperglycemia promotes an aggressive phenotype in breast cancer cells
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ABSTRACT:
PROVIDER: PRJNA561818 | ENA |
REPOSITORIES: ENA
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Project description:Diabetes and breast cancer are common diseases with a major impact on the health sector in Mexico and worldwide. Epidemiological and experimental works support the link between type 2 diabetes and breast cancer; these data support that insulin resistance, hyperglycemia, hyperinsulinemia, and elevated levels of IGF-1 in patients with type II diabetes mellitus promote growth and invasiveness of tumor cells. The aim of the present work was to determine, by microarray, the mechanisms of action and signaling of a hyperglycemic microenvironment in the cell line (MDA-MB-231) and its effect to treatment with cisplatin (CCP). MDA-MB-231 breast cancer cells were cultured in DMEM medium, supplemented with 10% fetal bovine serum and antibiotics at 5% CO2, at 37 ˚C. We proceeded to extract total RNA for the analysis of microarrays under LG (low glucose) and HG (high glucose) conditions; for the cDNA synthesis, it was labeled with dUTP-Cy3 or dUTP-Cy5 fluorophores, using a CyScribe Firs-Strand cDNA kit. The analysis was carried out through the KEGG pathways program; some bioenergetic metabolism processes (glycolysis, biosynthesis of purines and pyrimidines, and metabolism of glycerol phospholipids) were found altered, which fulfill the feedback function to the cellular microenvironment, activating some signaling processes, such as the Hippo route, PI3K-Akt, Jak-STAT, MAPK, Ras, Wnt/β-catenin, apoptosis, and favoring an aggressive phenotype and drug resistance in a hyperglycemic microenvironment. The microarray analysis was validated by qRT-PCr of the tetraspanin and Frizzled genes.
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Project description:We report that EVs originated from cancer cells can modulate glucose metabolism in the recipient cancer cells and induce cell proliferation and aggressive phenotype. Two breast cancer cell lines with different levels of glycolytic activity, MDA-MB-231 of a claudin low-type breast cancer cell and MCF7 of luminal type breast cancer cell, were selected and co-cultured, as the originating and recipient cells using indirect co-culture system such as transwell system or microfluidic system. Proteomic profiling of the co-cultured MCF7 cells revealed proliferation and dedifferentiation of the MCF7 cells following co-culture with the MDA-MB-231 cells. Transcriptomic analysis demonstrated that glycolysis increased in the co-cultured MCF7 cells, and the component analysis of glycolysis-related genes revealed that the second-most component after cytoplasm was extracellular exosomes. In addition, 36 significant KEGG pathways were identified in a total of 856 proteins identified by proteomin analysis of MDA-MB-231-induced EVs. Among these pathways were the main pathways (glycolysis/gluconeogenesis, pyruvate metabolism, and PI3K-Akt signaling pathways) that could explain the metabolic modulation of MCF7 cells. In our work, we indirectly show that it is MDA-MB-231-derived EVs that play an important role in this phenomenon. Our study highlights the potential effects of aggressive cancer cells on other surrounding cancer cells through EVs.
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