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. Author manuscript; available in PMC: 2013 Aug 24.
Published in final edited form as: Mol Cell. 2012 Jul 19;47(4):570–584. doi: 10.1016/j.molcel.2012.06.014

Figure 5. An IL-6 inflammatory loop mediates trastuzumab resistance through autocrine and paracrine mechanisms.

Figure 5

(A and B) When co-cultured with BT474-PTEN-LTT cells for two weeks, parental BT474-DsRed cells acquired a CD44+CD24− phenotype a transition which was inhibited by addition of anti-IL-6R antibody at the beginning of co-culture. However once cells acquired the CD44+/CD24− phenotype they became resistant to anti-IL-6R antibody (late). (B and C) Conditioned medium (CM) from BT474-PTEN-LTT cells or recombinant IL-6 was able to induce mesenchymal phenotype and CD44 expression in both parental BT474-DsRed and SKBR3-DsRed cells. (D) CM from BT474-PTEN-LTT cells or recombinant human IL-6 increased the sphere formation of BT474-DsRed cells providing resistance to trastuzumab an effect that was reversed by anti-IL-6R antibody. (E) Trastuzumab reduced the number of viable BT474-DsRed cells by 50%, while it had no effect on the viability of BT474-PTEN− cells or BT474-DsRed cells when they were grown in the presence of CM or IL-6, an effect reversed by anti-IL-6R antibody. (See Figure S2). Error bars represent the mean and standard deviation of two independent experiments performed in duplicate samples. (*p ≤ 0.05, #p ≤ 0.01).