Expression level and potential target pathways of miR-1-3p in colorectal carcinoma based on 645�cases from 9 microarray datasets

Abstract

For the purpose of demonstrating the clinical value and unraveling the molecular mechanisms of micro RNA (miR)-1-3p in colorectal carcinoma (CRC), the present study collected expression and diagnostic data from Gene Expression Omnibus (GEO), ArrayExpress and existing literature to conduct meta-analyses and diagnostic tests. Furthermore, the potential targets of miR-1-3p were attained from datasets that transfected miR-1-3p into CRC cells, online prediction databases and differentially expressed genes from The Cancer Genome Atlas and literature. Subsequently, bioinformatics analysis was conducted based on the aforementioned selected target genes. As a result, downregulation of miR-1-3p was observed. The combined standardized mean difference was −0.51 with 95% confidence interval (CI) of −0.68 to −0.33 using a fixed effect model, which demonstrated a significant downregulation of miR-1-3p in CRC. The combined sensitivity, specificity, positive likelihood ratio, negative likelihood ratio diagnostic score and odds ratio were 0.74 (95%CI: 0.48, 0.90), 0.75 (95%CI: 0.35, 0.94), 2.94 (95%CI: 1.01, 8.55), 0.34 (95%CI: 0.19, 0.60), 2.15 (95%CI: 1.06, 3.23) and 8.57 (95%CI: 2.89, 25.36). The summarized receiver operating characteristic curve demonstrated that the area under the curve was 0.81. In bioinformatics analyses based on 30 promising targets, the most enriched terms in Gene Ontology were positive regulation of transcription from RNA polymerase II promoter, extracellular region and transcription factor binding. Kyoto Encyclopedia of Genes and Genomes pathway analysis highlighted the pathway termed cytokine-cytokine receptor interaction. In protein-protein interaction analysis, platelet factor 4 was selected as the hub gene. To conclude, miR-1-3p is downregulated in CRC and likely suppresses CRC via multiple biological approaches, which indicates the diagnostic potential and tumor suppressive efficacy.

<p>miR-1-3p suppresses the epithelial-mesenchymal transition property in renal cell cancer by downregulating Fibronectin 1</p>

“…Previous studies have clarified the irregular expression levels of several miRNAs in RCC together with miR-1-3p. miR-1-3p have been validated to be reduced in numerous different types of cancer, including lung cancer,54 colorectal carcinoma55, and urinary neoplasms. But the role and function of miR-1-3p in malignancy disease have not been definitely illuminated.…”

“…But the role and function of miR-1-3p in malignancy disease have not been definitely illuminated. Wang et al, revealed that miR-1-3p inhibit lung cancer by c-Met signaling and EMT process 55. Gao et al, demonstrated that miR-1-3p inhibits cell proliferation and invasion by regulating the BDNF-TrkB signaling pathway in bladder cancer 56.…”

<p>miR-1-3p suppresses proliferation of hepatocellular carcinoma through targeting SOX9</p>

“… 23 miR-1-3p is downregu-lated by hypoxia in pulmonary artery smooth muscle cells and contributes to the development of pulmonary vascular remodeling. 24 miR-1-3p was downregulated in various types of cancer, such as prostate cancer, 25 oral squamous cell carcinoma (OSCC), 26 bladder cancer, 27 colorectal carcinoma, 28 and lung cancer, 29 where miR-1-3p regulated the proliferation and invasion.…”

The putative tumour suppressor miR-1-3p modulates prostate cancer cell aggressiveness by repressing E2F5 and PFTK1

“…It has been shown that ectopic expression of miR-1 inhibits prostate cancer cell growth, epithelial-mesenchymal transition and bone metastasis [ 18 , 19 ]. In addition, miR-1-3p has been reported to suppress tumor growth in colon carcinomas [ 20 ], decrease cellular proliferation and migration of oral squamous cell carcinoma [ 21 ], inhibit cell proliferation and invasion and induce apoptosis in bladder cancers [ 22 ]. These data indicate a potential tumor suppressive function of miR-1-3p.…”