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. 2017 Feb 15;8(13):20813–20824. doi: 10.18632/oncotarget.15343

Figure 1. Post-translational modifications of kinesins and NuMA identified by changes in their isoelectric point in human cells treated with phenanthrenes.

Figure 1

(A) The isoelectric point of kinesins HSET/kifC1 and kif18A in human triple negative breast cancer cells MDA-MB-231 was shifted towards higher pH values (less negatively charged protein) after 27 hours incubation with the phenanthrene derivatives PJ34 (20 μM), Tiq-A (50 μM) or Phen (50 μM). No similar effect was induced by the non-phenanthrene PARP1 inhibitor ABT888 (20 μM). (B) The isoelectric point of α-tubulin was not affected by the phenanthrenes or by ABT888 in MDA-MB-231 cells. (C) The isoelectric point of kinesins HSET/kifC1 and kif18A was shifted towards higher pH values (less negatively charged protein) in human lung (A549), pancreas (PANC1) and glioblastoma (U87) cancer cells incubated for 27 h with PJ34 (20 μM), Tiq-A (50 μM) or Phen (50 μM). No similar effect on their isoelectric point was induced by the non-phenanthrene PARP1 inhibitor ABT888 (20 μM). (D) Treatment with the phenanthridine PJ34 (20 μM, 27 h) did not affect the isoelecrtic point of α-tubulin and kinesins HSET/kifC1 and Kif18A in human normal breast epithelial cells MCF10A. The isoelectric point of NuMA was shifted towards lower pH (more negatively charged protein) in these cells. (E) Treatment with PJ34 (20 μM, 27 h) shifted the isoelectric point of NuMA towards higher pH values (less negatively charged protein) in human malignant cells, including: breast (MDA-MB-231), lung (A549), pancreas (PANC1) and glioblastoma (U87) cells. Representative results of 4 different experiments in each cell type are displayed in A–E.