Abstract
Alterations in the Checkpoint kinase (CHEK1) gene, its regulation, and the possible clinical outcomes in human solid tumors have not been previously examined. Therefore, the present study was carried out to evaluate the expression of CHEK1 in solid tumors as well as the mechanism by which it can be regulated through non-coding RNAs. The expression of CHEK1 was investigated using Oncomine analysis. cBioPortal, Kaplan–Meier Plotter, and PrognoScan were performed to identify the prognostic roles of this gene in solid tumors. The copy number alteration, mutation, interactive analysis, and visualization of the altered networks were performed by cBioPortal. The molecular binding analysis was carried out by Schrodinger suite, PATCHDOCK, and discovery studio visualizer. The study demonstrated that the CHEK1 gene was differentially expressed in four different cancers, and that reduced CHEK1 mRNA expression is an unfavorable prognostic factor for patients with gastric and colorectal cancer. The molecular docking results showed that the CHEK1 gene can be regulated by microRNAs (miR-195-5p) due to the number of stable hydrogen atoms observed within the distance of 2.0 Å and the favorable amino acids (Ala221, Ile353, Ile365, Ile756, Val797, Val70, Val154, Ile159, Val347, Tyr804, Phe811, Tyr815, and Phe156) identified in the binding pocket of the argonaute protein. Due to the possibility of CHEK1’s involvement in solid tumors, it may potentially be a target for therapeutic intervention in cancer. Further studies into the interaction between CHEK1 and other co-expressed genes may give further insight into other modes of regulation of this gene in cancer patients.
Highlights
Carcinogenesis is the development of a malignant tumor in healthy tissues resulting from a complex series of events beginning with a single cell that has acquired malignant properties through genetic or epigenetics alterations
This study extensively investigated the role of checkpoint kinase 1 (CHEK1) in solid tumors as well as the mechanism by which it can be regulated through molecular docking with human argonaute protein assisted by a known microRNA
Together with the fatal effects of its deficiency in mammals, it could be used to explain the paucity of cancer-associated alterations of CHEK1
Summary
Carcinogenesis is the development of a malignant tumor in healthy tissues resulting from a complex series of events beginning with a single cell that has acquired malignant properties through genetic or epigenetics alterations. Cancers result from a progressive accumulation of genetic alterations (mutations) in many different genes. These mutations include alteration of the copy number, translocation events, base insertion, duplication, deletions, and substitutions [1,2,3]. All cancers, including solid tumors, display recurrent chromosomal abnormalities. The exact biological significance relating to gene expression alterations in important genes remains unclear in solid tumors. Advances in the understanding of genetic alterations associated with solid tumors are retarded because
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