Abstract
Polo-like kinase 1 (PLK1) is a multi-functional protein and its aberrant expression is a driver of cancerous transformation and progression. To increase our understanding of the clinical value and potential molecular mechanism of PLK1 in gastric cancer (GC), we performed this comprehensive investigation. A total of 25 datasets and 12 publications were finally incorporated. Additional immunohistochemistry was conducted to validate the expression pattern of PLK1 in GC. The pooled standard mean deviation (SMD) indicated that PLK1 mRNA was up-regulated in GC (SMD=1.21, 95% CI: 0.65-1.77, P< 0.001). Similarly, the pooled odds ratio (OR) revealed that PLK1 protein was overexpressed in GC compared with normal gastric tissue (OR=12.12, 95% CI: 5.41-27.16, P<0.001). The area under the curve (AUC) of the summary receiver operating characteristic (SROC) curve was 0.86. Furthermore, our results demonstrated that GC patients with PLK1 overexpression were significantly associated with unfavorable overall survival (HR =1.54, 95% CI: 1.30–1.83, P<0.001), lymph node metastasis (OR = 1.78, 95% CI: 1.13–2.80, P=0.013) and advanced TNM stage (OR=1.48, 95% CI: 1.02-2.15, P=0.038). Altogether, 100 similar genes were identified by Gene Expression Profiling Interactive Analysis (GEPIA) and further with gene-set enrichment analysis. These genes were related to gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways relevant to the cell cycle. Gene set enrichment analysis (GSEA) indicated that PLK1 is associated with various cancer-related pathways. Collectively, this study suggests that PLK1 overexpression could play vital roles in the carcinogenesis and deterioration of GC via regulating tumor-related pathways.
Highlights
Gastric cancer (GC) is the fourth leading human cancer, and it ranks as the second most common cause of tumor-related mortality all over the world, seriously threatening human health [1]
Our results demonstrated that gastric cancer (GC) patients with Polo-like kinase 1 (PLK1) overexpression were significantly associated with unfavorable overall survival (HR =1.54, 95% confidence interval (CI): 1.30–1.83, P
We investigated the expression pattern of PLK1 in gastric cancer based on each independent dataset
Summary
Gastric cancer (GC) is the fourth leading human cancer, and it ranks as the second most common cause of tumor-related mortality all over the world, seriously threatening human health [1]. Diagnostic and therapeutic techniques of GC have made advances over the past decades, the mortality rate is still fairly high due to its aggressive behavior [3,4,5,6]. Because clinically applicable biomarkers are fairly meager, exploring novel, effective molecular biomarkers to elucidate effective therapeutic targets for GC patients is still imperative. Prior to our study, increasing evidence has suggested that dysregulated expressions of PLK1 exerted indispensable functions in GC progression. Otsu H suggested that GC patients with high expression of PLK1 and DNA aneuploidy had inferior survival outcome [15]. Elevated PLK1 promotes GC cell metastasis rates and epithelial-mesenchymal transition by regulating the activation of the protein kinase B pathway [16]. Despite several independent studies providing various valuable perspectives of PLK1 in GC, low numbers of studies have led to a limited ability to uncover the complexity of GC and no meta-analysis to clarify the reliability and extent of its clinical value in GC has been performed
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
