Anti-PLK2 (aa 666-685) polyclonal antibody

Aberrant activation of kinases has emerged to be a key event along with tumor progression, maintenance of tumor phenotype and response to anticancer treatments. This study documents the existence of an oncogenic autoregulatory feedback loop that includes the polo-like kinase-2 (Snk/Plk2) and mutant p53 proteins. Plk2 protein binds to and phosphorylates mutant p53, thereby potentiating its oncogenic activities. Phosphorylated mutant p53 binds more efficiently to p300, consequently strengthening its own transcriptional activity. Plk2 gene is regulated at a transcriptional level by both wt- and mutant p53 proteins. This leads to growth suppression or enhanced cell proliferation and chemo-resistance, respectively. In turn, the siRNA-mediated knockdown of either mutant p53 or Plk2 proteins significantly curtails the growth properties of tumor cells and their chemo-resistance to anticancer treatments. Therefore, this paper identifies a novel tumor network including Plk2 and mutant p53 proteins whose triggering in response to DNA damage might disclose important implications for the treatment of human cancers.

Colorectal cancer (CRC) is one of the most common malignances worldwide. Chemoresistance remains a major issue in the field of CRC treatment. The present study aimed to investigate the potential role of polo-like kinase 2 (Plk2) in chemoresistance in CRC. The associations between Plk2 and clinicopathological factors, as well as chemotherapeutic benefit were analyzed with a publicly available CRC dataset. The correlation between Plk2 expression and chemosensitivity was further confirmed in CRC cells. Moreover, knockdown and exogenous overexpression experiments of Plk2 were carried out to uncover the potential role of Plk2 in regulating the chemoresistance of CRC cells. We found that the expression of Plk2 was significantly associated with proximally located tumors. In addition, it was found that high expression ofPlk2 was associated with deficient mismatch repair status, B-raf serine/threonine kinase proto-oncogeneand Kirsten rat sarcoma viral oncogene homolog mutations. By contrast, tumor protein 53 mutation was correlated with a low expression level of Plk2. A higher expression level of Plk2 significantly predicted a poorer outcome in patients with CRC. However, the prognostic significance was only observed in patients who received adjuvant chemotherapy. In CRC cells, higher levels of Plk2 were associated with increased resistance to chemotherapeutic agents. Knocking down the expression of Plk2 resulted in elevated cellular apoptosis induced by oxaliplatin. By contrast, exogenous overexpression of Plk2 exerted an anti-apoptotic effect and enhanced the resistance of CRC cells to chemotherapeutic agents. In conclusion, a high expression of Plk2 was associated with chemoresistant traits of CRC through inhibiting apoptosis. These results suggested that Plk2 may serve as a predictive marker for chemoresistance and a novel target in CRC treatment.