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<p>Abnormal expression of polo-like kinase 2 (PLK2) has been identified in various cancers and is correlated with disease progression, chemoresistance, prognosis, and recurrence. However, the clinical significance of abnormal PLK2 expression in acute myeloid leukemia (AML) has not been explored fully. The present investigation explored the PLK2 expression status and clinical significance in AML. PLK2 mRNA transcript was significantly higher in AML patients than in controls determined by public database analysis and real-time quantitative PCR validation. The clinical significance of PLK2 expression was assessed in AML cohorts from The Cancer Genome Atlas, the Gene Expression Omnibus and our hospital. The results of ROC curve analysis suggested that PLK2 transcript levels could be a potential indicator for AML diagnosis both in total AML and cytogenetically normal AML patients. Abnormal PLK2 expression was associated with specific subtypes in AML. High PLK2 expression was more common in FAB-M5 subtype and less frequent in favorable karyotypic/molecular risks. Patients with high PLK2 expression had a higher incidence of NPM1/DNMT3A mutations but a lower frequency of TP53/CEBPA mutations. PLK2 overexpression was an adverse prognostic indicator of overall survival for AML patients. Furthermore, patients with high PLK2 expression may profit more from transplantation than those without, suggesting PLK2 expression may have potential to help hypothesis-generating for HSCT decision support in AML. Additionally, PLK2 expression was strongly negatively correlated with PLK2 methylation both in AML patients, primary and demethylation-treated AML cells, indicating PLK2 expression is regulated by its promoter methylation. Bioinformatics analysis demonstrated high PLK2 expression was positively associated with oncogenes such as FAM163A, CTNND2, DAAM2, PITX1, POU1F1, mir-196a and negatively associated with tumor suppressors such as EMX2, PADI3, CDO1, SHOX2 and mir-508. In conclusion, the research elaborates on the expression profile and the clinical significance of PLK2 gene in AML, suggesting PLK2 expression may help risk stratification and hypothesis-generating for HSCT decision support.</p>

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Abnormal PLK2 expression is associated with specific subtypes and may help risk stratification in acute myeloid leukemia

  • 期刊论文

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  • 发表日期：

    2026年1月13日

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  • Qin Chen,
  • Zijun Xu,
  • Tingting Du,
  • Wei Zhao,
  • Dongming Yao,
  • Haoxi Ni

摘要

Abnormal expression of polo-like kinase 2 (PLK2) has been identified in various cancers and is correlated with disease progression, chemoresistance, prognosis, and recurrence. However, the clinical significance of abnormal PLK2 expression in acute myeloid leukemia (AML) has not been explored fully. The present investigation explored the PLK2 expression status and clinical significance in AML. PLK2 mRNA transcript was significantly higher in AML patients than in controls determined by public database analysis and real-time quantitative PCR validation. The clinical significance of PLK2 expression was assessed in AML cohorts from The Cancer Genome Atlas, the Gene Expression Omnibus and our hospital. The results of ROC curve analysis suggested that PLK2 transcript levels could be a potential indicator for AML diagnosis both in total AML and cytogenetically normal AML patients. Abnormal PLK2 expression was associated with specific subtypes in AML. High PLK2 expression was more common in FAB-M5 subtype and less frequent in favorable karyotypic/molecular risks. Patients with high PLK2 expression had a higher incidence of NPM1/DNMT3A mutations but a lower frequency of TP53/CEBPA mutations. PLK2 overexpression was an adverse prognostic indicator of overall survival for AML patients. Furthermore, patients with high PLK2 expression may profit more from transplantation than those without, suggesting PLK2 expression may have potential to help hypothesis-generating for HSCT decision support in AML. Additionally, PLK2 expression was strongly negatively correlated with PLK2 methylation both in AML patients, primary and demethylation-treated AML cells, indicating PLK2 expression is regulated by its promoter methylation. Bioinformatics analysis demonstrated high PLK2 expression was positively associated with oncogenes such as FAM163A, CTNND2, DAAM2, PITX1, POU1F1, mir-196a and negatively associated with tumor suppressors such as EMX2, PADI3, CDO1, SHOX2 and mir-508. In conclusion, the research elaborates on the expression profile and the clinical significance of PLK2 gene in AML, suggesting PLK2 expression may help risk stratification and hypothesis-generating for HSCT decision support.