IL-1[beta] induces up-regulation of BIRC3 , a gene involved in chemoresistance to doxorubicin in breast cancer cells

• Published in: Cancer letters Vol. 390; p. 39
• Main Authors: Mendoza-Rodríguez, Mónica, Arévalo Romero, Haruki, Fuentes-Pananá, Ezequiel M, Ayala-Sumuano, Jorge-Tonatiuh, Meza, Isaura
• Format: Journal Article
• Language: English
• Published: Clare Elsevier Limited 01-04-2017
• Subjects: Acquisitions & mergers; Apoptosis; Breast cancer; Cell cycle; Cloning; Conflicts of interest; Cytokines; Gene expression; Immunoglobulins; Kinases; Medical prognosis; Membranes; Metastasis; Proteins; Tumors; United States > US
• DOI: 10.1016/j.canlet.2017.01.005
• EISSN: 1872-7980
• ISSN: 0304-3835

Epithelial to mesenchymal transition (EMT) of tumor cells facilitates their progress to metastasis. In the tumor microenvironment the inflammatory cytokine 1β (IL-1β) has been associated with tumor development and invasiveness. IL-1β-induced EMT triggers the expression of markers associated with malignancy. We have recently reported that an IL-1β-highly responsive clone (6D cells) from non-invasive MCF-7 breast cancer cells activates PI3K/Rac and IL-1RI/β-catenin pathways that up-regulate the transcription of genes involved in an EMT-like process. However, a correlation between the EMT program induced by a pro-inflammatory environment, and the acquisition of chemoresistance has not been yet determined in these cells. In this work, we report the expression of cell survival genes after IL-1β stimulation of 6D cells. The expression ofCDKN1A,TP63,SFNand, particularly,BIRC3was found to be up-regulated in a RNA-seq analysis and validated by qPCR. Cells stimulated with IL-1β when challenged with doxorubicin showed resistance to the drug, whereas silencing of BIRC3 decreased viability of the cells treated with the drug. Our present results show that IL-1β confers doxorubicin resistance to breast cancer cells, underlining the importance of an inflammatory environment in cancer malignancy.