Abstract
Overexpression of the miR-31-5p contributes to tumorigenesis and metastasis in diverse neoplasms. In this study, we evaluated expression of miR-31-5p in patients with colon adenocarcinoma (COAD). We found that miR-31-5p was overexpressed in four cohorts (GSE30454, GSE41655, GSE18392, GSE108153) of COAD patients. Importantly, a LinkedOmics analysis revealed that high miR-31-5p expression was associated with poor overall survival of COAD patients. At total of 133 putative target genes of miR-31-5p were identified from TargetScan, miRDB, and TargetMiner. After integrating the target genes with 1,556 deregulated genes in COAD, 8 were acquired that may be targeted by miR-31-5p and contribute to COAD progression. Among these, tensin 1 (TNS1) showed the greatest prognostic ability in COAD and was strongly correlated with M2 macrophages, regulatory T cells, and other immune cells. These findings indicate that, in COAD, miR-31-5p is a potential prognostic factor that affects immune infiltration by targeting TNS1.
Highlights
Colorectal cancer (CRC) is a common malignancy throughout the world
To evaluate the expression level of miR-31-5p in various cancers, we performed a systematic pancancer analysis based on The Cancer Genome Atlas (TCGA) and Genotype-Tissue Expression (GTEx) miRNA databases
The results showed that miR-31-5p is overexpressed in many tumor types, including CRC, breast cancer, lung squamous cell carcinoma, liver hepatocellular carcinoma, and head and neck cancer (Figure 1A)
Summary
Colorectal cancer (CRC) is a common malignancy throughout the world. Colon adenocarcinoma (COAD), which accounts for 90% of all CRCs, is the most common histologic subtype [3]. MicroRNAs (miRNAs), a family of noncoding RNAs, are prevalent in multicellular and complex eukaryotes and participate in various physiologic processes of cells, including posttranscriptional regulation of gene expression [5, 6]. MiRNAs regulate various biologic processes of tumor cells, including proliferation, migration, and apoptosis [7, 8]. Aberrant expression of miRNAs contributes to development and progression of COAD [9]. The strong evidence that dysregulation of miRNAs contributes to COAD pathogenesis provides a rationale for targeting miRNAs in cancer treatment
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