Downregulation of miR­486­5p in papillary thyroid carcinoma tissue: A study based on microarray and miRNA sequencing.

Abnormal expression of microRNA (miR) is associated with the occurrence and progression of various types of cancers, including papillary thyroid carcinoma (PTC). In the present study, the aim was to explore miR­486­5p expression and its role in PTC, as well as to investigate the biological function of its potential target genes. The expression levels of miR­486­5p and its clinicopathological significance were examined in 507 PTC and 59 normal thyroid samples via The Cancer Genome Atlas (TCGA). Subsequently, the results were validated using data from Gene Expression Omnibus (GEO) and ArrayExpress. Receiver operating characteristic and summary receiver operating characteristic curves were used to assess the ability of miR­486­5p in distinguishing PTC from normal tissue. Furthermore, potential miR­486­5p mRNA targets were identified using 12 prediction tools and enrichment analysis was performed on the encoding genes using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes. The expression levels of miR­486­5p were consistently downregulated in PTC compared with in normal tissue across datasets from TCGA, GEO (GSE40807, GSE62054 and GSE73182) and ArrayExpress (E­MTAB­736). The results also demonstrated that miR­486­5p expression was associated with cancer stage (P=0.003), pathologic lymph node (P=0.047), metastasis (P=0.042), neoplasm (P=0.012) and recurrence (P=0.016) in patients with PTC. In addition, low expression of miR­486­5p in patients with PTC was associated with a worse overall survival. A total of 80 miR­486­5p­related genes were observed from at least 9 of 12 prediction platforms, and these were involved in 'hsa05200: Pathways in cancer' and 'hsa05206: MicroRNAs in cancer'. Finally, three hub genes, CRK like proto­oncogene, phosphatase and tensin homolog and tropomyosin 3, were identified as important candidates in tumorigenesis and progression of PTC. In conclusion, it may be hypothesized that miR­486­5p contributes towards PTC onset and progression, and may act as a clinical target. However, in vitro and in vivo experiments are required to validate the findings of the present study.

Comprehensive analysis of the clinical significance and prospective molecular mechanisms of differentially expressed autophagy-related genes in thyroid cancer.

Thyroid cancer (TC) is the most common endocrine malignancy, accounting for approximately 90% of all malignancies of the endocrine system. Despite the fact that patients with TC tend to have good prognoses, the high incidence rate and lymph node metastases remain unresolved issues. Autophagy is an indispensable process that maintains intracellular homeostasis; however, the role of autophagy in several steps of the initiation and progression of TC has not yet been elucidated. In this study, we first identified several autophagy-related genes (ARGs) that were provoked in the onset of TC. Subsequently, a bioinformatics analysis hinted that these genes were markedly disturbed in several proliferative signaling pathways. Moreover, we demonstrated that the differentially expressed ARGs were closely related to several aggressive clinical manifestations, including an advanced tumor stage and lymph node metastasis. Our study further selected prognostic ARGs and developed a prognostic signature based on three key genes (ATG9B, BID and B1DNAJB1), which displayed a moderate ability to predict the prognosis of TC. On the whole, the findings of this study demonstrate that ARGs disrupt proliferation-related pathways and consequently lead to aggressive clinical manifestations. These findings provide insight into the potential molecular mechanisms of action of ARGs and their clinical significance, and also provide classification information of potential therapeutic significance.