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. 2019 Feb 20;17(4):3981–3989. doi: 10.3892/ol.2019.10059

Figure 1.

Figure 1.

Inhibition of the STAT3 signaling pathway by ruxolitinib in TAMR-MCF-7 cells. (A) Expression of pSTAT3 and STAT3 in MCF-7 and TAMR-MCF-7 cells. β-actin levels were utilized as the loading controls. (B) Inhibition of STAT3 phosphorylation by ruxolitinib. MCF-7 and TAMR-MCF-7 cells were treated with vehicle or ruxolitinib (0.1–10 µM) for 24 h. (C) Effects of ruxolitinib on the expression of downstream target genes of the JAK-STAT pathway. The protein levels of c-Myc, c-Jun, Cyclin B1, Cyclin D1, Bcl-2 and HIF-1α were determined in MCF-7 and TAMR-MCF-7 cells 24 h following ruxolitinib treatment (0.1–10 µM). All of the experiments were repeated at least three times. JAK, Janus kinase; STAT, signal transducer and activator of transcription; pSTAT, phosphorylated STAT; HIF-1α, hypoxia inducible factor-1α; Bcl-2, B-cell lymphoma 2; TAMR, tamoxifen resistant.