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. 2019 Oct 10;11(10):1527. doi: 10.3390/cancers11101527

Figure 8.

Figure 8

The effects of ivermectin, a PAK1 inactivator, on CSC loads in breast cancer. (A) Transcriptional levels of Sox2, Oct4, CD44, c-Myc, and Nanog genes were analyzed in ivermectin-treated mammospheres using specific primers. β-actin was used as a control. (B) Effect of ivermectin on mammosphere growth. Ivermectin treatment prevents mammosphere proliferation. Ivermectin-treated mammospheres were dissociated into single cells and plated in 6-well plates in equal numbers. Twenty-four hours after plating, the cells were counted. Two and 3 days later, the cells were counted. The data are presented as the mean ± SD; n = 3; * p < 0.05 vs. control. (C) The proposed model for CSC formation by JAK2/PAK1/Stat3/IL-6. IL-6-induced JAK2 and PAK1 interaction. JAK2 inhibitor (TG101209) and PAK1 inactivator (ivermectin) treatment blocks the Stat3 signaling pathway and IL-6 gene expression and inhibits CSC formation. TG101209 and ivermectin treatment reduces extracellular IL-6 and Stat3 signaling. Extracellular IL-6 induces the conversion of cancer cells to CSCs. PAK1/Stat3 regulates CSC formation through Stat3 signaling and extracellular IL-6.