fig3

MEK inhibition activates STAT signaling to increase breast cancer immunogenicity via MHC-I expression

Figure 3. MEKi-induced MHC-I & PD-L1 expression are STAT dependent in MMTV-Neu and E0771 cells. A: MMTV-Neu cells were reverse transfected with siRNAs against a non-targeting control (siNTC), STAT1, STAT3, or STAT5a prior to treatment with or without trametinib (50 nM; MEKi) for 72 h prior to flow cytometry analysis for MHC-I (H2Kq) and PD-L1 expression; (n = 3); B: E0771 cells were similarly transfected and treated as in A prior to flow cytometry analysis for MHC-I (H2Kb). MEKi: MEK inhibition; DMSO: dimethylsulfoxide

Cancer Drug Resistance
ISSN 2578-532X (Online)

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