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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: Mol Cancer Ther. 2016 Jun 21;15(7):1427–1435. doi: 10.1158/1535-7163.MCT-15-0897

Figure 2. Examples of how Plk1-associated kinase activity contributes to therapy resistance.

Figure 2

(A) Plk1 phosphorylation of its substrates GTSE-1 and Topors causes p53 inactivation which results in doxorubicin resistance (25, 26). (B) Plk1-associated kinase activity drives DNA replication under stress via modulating its substrates Hbo1 and Orc2, resulting in acquired gemcitabine resistance in pancreatic cancer cells (32, 34, 35). (C) Plk1 contributes to paclitaxel resistance by phosphorylating its substrates CLIP-170, p150Glued and Sgt1, thereby regulating microtubule dynamics and microtubule-kinetochore attachment (41-44). (D) Plk1-associated activation of AR signaling leads to ASI resistance in CRPC (47, 49). (E) Plk1 elevation causes inactivation of PTEN to modulate the metabolism in prostate cancer cells (56). (F) Inhibition of Plk1 enhances the efficacy of anti-neoplastic activity of metformin in prostate cancer via both p53 and metabolic pathways (52).