Abstract
The most prevalent malignant central nervous system (CNS) cancer is glioblastoma multiforme (GBM). PLKs (polo-like kinases) are a kind of serine-threonine kinase that modulate DNA replication, mitosis, and stress responses. PLKs in GBM need to be better studied and examined in terms of their expression, function, along with prognostic significance. Using an existing publicly available data set, we evaluated the expression level and prognostic relevance of PLKs in GBM patients at the molecular level. The biological processes along with cascades of the screened gene were predicted using the functional enrichment of Gene Set Enrichment Analysis, Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes pathways. The data illustrated that PLK1/3/4 contents were greater in GBM tissues than in non-tumorous tissues, but PLK2/5 expression levels were lower. PLK2 expression was also linked to patient outcome in GBM. Our findings imply that PLKs might be useful molecular indicators as well as prospective treatment targets for GBM. A PLK2 inhibitor has been studied for the first time in a glioma cell in this work. In glioma cells, ON1231320 has anticancer effects. Finally, a summary of PLK inhibitors is presented, along with projections for future progress.
Highlights
glioblastoma multiforme (GBM) is the most frequent malignant central nervous system (CNS) cancer in adults, which accounts for 55% of all gliomas [1]
The transcript expression levels of PLK1/3/4 were remarkably elevated in individuals with GBM, and that of PLK2 was remarkably downregulated in patients with GBM
The data illustrated that the contents of PLK1/3/4 were higher in GBM tissues than in non-tumorous tissues, whilst the contents of PLK2 and PLK5 were lower in GBM (Figure 1C)
Summary
GBM is the most frequent malignant CNS cancer in adults, which accounts for 55% of all gliomas [1]. Radiation and chemotherapy constitutes the current standard of treatment. The median time of survival is about 18 months, the survival rate is still poor [2]. Based on high-throughput genetic, genomic, and epigenetic data, several key molecules have been identified that contribute to GBM carcinogenesis and the development of targeted therapies for individual subtypes. Targeted therapies for specific mutations or subtypes have mostly failed due to the complexity of molecular heterogeneity within tumors [3]
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