Enhanced polo-like kinase 1 expression in myelodysplastic syndromes
- Author:
Kyoung Il MIN
1
;
Silvia PARK
;
Seung Hwan SHIN
;
Yong Rim KWON
;
Hye Joung KIM
;
Yoo Jin KIM
Author Information
- Publication Type:Original Article
- Keywords: Myelodysplastic syndromes; Polo-like kinase 1; Protein-serine-threonine kinases; DNA methylation; Gene expression
- MeSH: Bone Marrow; Cell Cycle; Cell Proliferation; Classification; DNA Methylation; Gene Expression; Humans; Karyotype; Leukemia; Leukemia, Myeloid, Acute; Lymphoma; Myelodysplastic Syndromes; Phosphotransferases; Protein-Serine-Threonine Kinases; Real-Time Polymerase Chain Reaction; RNA, Messenger; Up-Regulation
- From:Blood Research 2019;54(2):102-107
- CountryRepublic of Korea
- Language:English
- Abstract: BACKGROUND: Cancer is characterized by uncontrolled cellular proliferation, and Polo-like kinase 1 (PLK1), a key regulator of the cell cycle, is overexpressed in many cancers, including acute leukemia and lymphoma. However, the dynamics of PLK1 transcription in myelodysplastic syndromes (MDS) are unknown. This study aimed to investigate the transcript dynamics of PLK1 and determine its role in the pathophysiology of MDS. METHODS: PLK1 mRNA obtained from the bone marrow samples of 67 patients with MDS, 16 patients with secondary acute myeloid leukemia (sAML), and 10 healthy controls were analyzed using quantitative real-time PCR and compared according to various clinical parameters. RESULTS: The median PLK1 expression levels differed slightly, but not significantly, between MDS and sAML patients [661.21 (range, 29.38–8,987.31) vs. 1,462.05 (32.22–5,734.09), respectively], but were significantly higher (P<0.001) than the levels in the healthy controls [19.0 (1.60–49.90)]. Further analyses of PLK1 levels according to the WHO classification of MDS, prognostic risk groups, karyotype risk groups, marrow blast percentage, and depth of cytopenia did not reveal any significant associations. In patients progressing to sAML, PLK1 expression levels differed significantly according to the presence or absence of resistance to hypomethylation treatment (2,470.58 vs. 415.98, P=0.03). CONCLUSION: PLK1 is upregulated in MDS patients; however, its role in the pathophysiology of MDS is unclear. Gene upregulation in cases with pharmacotherapeutic resistance warrants further investigation.
