Abstract
Combinations of anticancer chemotherapeutics with glucocorticoids (GCs) are usually used to broaden the therapeutic range of main cytostatic agents and to diminish the side effects of chemotherapy. However, long-term GC administration leads to tumor resistance and the promotion of metastasis. GC effects are mediated by the glucocorticoid receptor, which regulates gene expression via DNA-dependent transactivation associated with GC side effects and therapeutically important transrepression. We aimed to determine the molecular markers associated with the GC-stimulated motility and migration of breast cancer cells. We showed that GCs stimulate the invasion and metastasis of breast cancer cells after 120 h of treatment and determined markers of GC-associated adhesion loss.
Supplementary Materials
The following are available online at https://www.mdpi.com/article/10.3390/IECBM2022-13379/s1.
Author Contributions
Conceptualization, E.L. and M.Y.; methodology, E.Z.; software, D.G.; validation, E.Z., D.G. and O.Z.; formal analysis, E.Z.; investigation, D.G.; resources, M.Y.; data curation, E.Z.; writing—original draft preparation, D.G.; writing—review and editing, E.L.; visualization, O.Z.; supervision, E.L.; project administration, M.Y.; funding acquisition, E.L. All authors have read and agreed to the published version of the manuscript.
Funding
Work was partially supported by RSCF (17-75-20124) and RFBR (16-04-01410, 15-04-04006).
Data Availability Statement
The data presented in this study are available on request from the corresponding author.
Conflicts of Interest
The authors declare no conflict of interest.
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