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• W3175017413 abstract "The aim of this study is to explore the resistance mechanisms to anti-epidermal growth factor receptor (EGFR) and anti-human epidermal growth factor receptor (HER2) targeted therapies in breast cancer (BC). Previous studies have implicated the microRNA (miR)-200 family in maintenance of the epithelial phenotype and sensitivity to EGFR targeted therapies and miR-221/222 have been associated with epithelial to mesenchymal transition (EMT), tumor progression and therapy resistance. To investigate mechanisms of EGFR/HER2 therapy resistance in breast cancer, therapy resistant variants of the therapy sensitive SKBR3 human breast cancer cell line were created by exposure to different concentrations of the EGFR/HER2 inhibitors lapatinib and gefitinib. Characterization of therapy sensitive and resistant variants of SKBR3 demonstrated that miR-200a is downregulated while miR-221 and miR-222 are overexpressed in the therapy resistant cells. Therefore, the current objective is to validate the role of these miRNAs in therapy resistance. The hypothesis is that re-expression of miR-200a and downregulation of miR-221/222 will help overcome therapy resistance to EGFR/HER2 targeted therapy. Therefore, we re-expressed miR-200a ectopically in the therapy resistant and sensitive cells using a lentiviral vector containing miR-200a, or a control vector. MiR-221/222 inhibition was achieved by expressing anti-miR-221/222 or control inhibitors. MTT assays were used to determine the IC50s for cell viability. Both SKBR3 parental and lapatinib resistant variants with ectopic expression of miR-200a were more sensitive to lapatinib treatment as shown by a decrease in the IC50 when treated with lapatinib. Therapy sensitive and resistant cell lines also demonstrated a decrease in cell viability when miR-221 or miR-222 was downregulated using miRNA inhibitors. In conclusion, overexpression of miR-200a or downregulation of miR- 221/222 family reduces the malignancy of SKBR3 parental cell lines and sensitizes EGFR/HER2 therapy resistant cells. These results suggest that manipulation of miR-200a, miR-221 and miR-222 can be used as therapeutic strategies in combination with HER2/EGFR therapy to reduce cancer malignancy and therapy resistance. Support or Funding Information This work was supported by grants from NIH/NIGMS SC3GM094824 to SD, RCMI Programs G12RR03051 to UPR MSC, MBRS Program RISE (R25GM061838) to LDB and MM, and Bright Cure Program (U54) University of Puerto Rico/MD Anderson Cancer Center to PRV. This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal." @default.
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• W3175017413 date "2019-04-01" @default.
• W3175017413 modified "2023-10-01" @default.
• W3175017413 title "Sensitization of Anti‐EGFR/HER2 Targeted Therapy Resistance in Breast Cancer Cells by MiRNA Manipulation" @default.
• W3175017413 doi "https://doi.org/10.1096/fasebj.2019.33.1_supplement.647.47" @default.
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