Departmental sources Background: Thyroid carcinoma is a malignancy with high morbidity and mortality. Genetic alterations play pivot roles in the pathogenesis of thyroid carcinoma, where long noncoding RNA (lncRNA) have been identified to be crucial. This study sought to investigate the biological functions of lncRNA expression profiles in thyroid carcinoma. Material/Methods: The lncRNAs expression profiles were acquired from The Cancer Genome Atlas (TCGA) database according to 510 thyroid cancer tissues and 58 normal thyroid tissues. By using R package edgeR, differentially expressed RNAs were obtained. Also, an overall survival model was established based on Cox regression and clinical data then testified by Kaplan-Meier plot, receiver operating characteristic (ROC)-curve and C-index analysis. We investigated the co-expressed genes with lncRNAs involved in the prognostic model, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis was conducted R package clusterProfile. Results: A total of 352 lncRNAs were identified as differentially expressed in thyroid carcinoma, and an overall survival model consisting of 8 signature lncRNAs was proposed (ROC=0.862, C-index=0.893, P<0.05), 3 of which (DOCK9-DT, FAM111A-DT, and LINC01736) represent co-expressed mRNAs. However, as an oncogene, only FAM111A-DT increased the prognostic risk in thyroid carcinoma. Furthermore, we found differential genes LINC01016, LHX1-DT, IGF2-AS, ND MIR1-1HG-AS1, significantly related to lymph node metastasis (P<0.05). Conclusions: In this study, we clarified the differential lncRNA expression profiles which were related to the tumorigenesis and prognosis in thyroid carcinoma. Our results provide new rationale and understandings to the pathogenesis and regulatory mechanisms of thyroid carcinoma.

Background: The effects of miR-524-5p on breast cancer (BC) have not been investigated, though studies show that miR-524-5p has an anticancer function. Thus, this study investigated the effects of miR-524-5p on BC cells and its potential molecular mechanism. Materials and Methods: The expression of miR-524-5p from the collected BC samples was determined. Cell counting kit-8 (CCK-8) assay was performed to examine the effect of miR-524-5p on BC cells viability. The target for miR-524-5p was predicted by bioinformatics and further verified by luciferase assay. Wound healing assay and transwell assay were performed to determine cell migration and invasion of BC cells. The expressions of Follistatin-like 1 (FSTL1) and related proteins in epithelial-mesenchymal transition (EMT) were detected by Western blotting and quantitative real-time polymerase chain reaction. Results: MiR-524-5p was low-expressed in BC samples, and upregulation of miR-524-5p suppressed BC cell viability, migration, and invasion. FSTL1 was predicted as a target for miR-524-5p. In addition, overexpressed FSTL1 effectively abolished the effect of miR-524-5p on inhibiting FSTL1 expression, and reversed the inhibitory effects of miR-524-5p on the migration, invasion of BC cells as well as the effect of miR-524-5p on regulating the expressions of matrix metalloproteinase 2 (MMP2), matrix metalloproteinase 9 (MMP9), E-cadherin, and N-cadherin. Conclusions: Our findings suggest that miR-524-5p targeting FSTL1 adversely affects the progression of migration, invasion, and EMT of BC cells, thus, miR-524-5p is possibly a target for BC treatment.

Introduction: Breast cancer is one of the most common malignant tumors in the United States. However, the molecular mechanism involved in the progression of breast cancer has remained unclear. Long non-coding RNAs (lncRNA) have been reported as key regulators in the progression and metastasis of cancer. Material and methods: In this study, we identified significantly differentially expressed mRNAs and lncRNAs in breast cancer using the GSE70947 dataset. Gene ontology (GO) and KEGG pathway was used to explore the key roles of differentially expressed lncRNAs in breast cancer. The dysregulated lncRNAs and mRNAs expression profiles in HER2-positive and ER-negative breast cancer were also analyzed in this study. Results: Our results showed that PVT1, LOC145837, FLJ40504 and FLJ45983 were significantly decreased in HER2-positive and ER-negative breast cancers. We also constructed the PVT1, LOC145837, FLJ40504 and FLJ45983 mediated cRNA networks in HER2-positive and ER-negative breast cancers. Moreover, using the Betastasis dataset, we found that high PVT1 expression levels were associated with a lower survival rate in breast cancer patients. Conclusions: These results elucidate the functions of lncRNAs and provide useful information for exploring therapeutic candidate targets and new molecular biomarkers for ER-negative and HER-2 enriched subtype breast cancer.

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