Non-functioning pituitary adenoma (NFPA) is a benign tumor arising from the adenohypophyseal cells. They can be associated with symptoms arising from mass effect. Although these tumors are regarded to be benign tumors, they are associated with increased comorbidity and mortality. Several studies have indicated abnormal expression of genes in these tumors. In the current study, we have used existing methods to identify differentially expressed genes (DEGs) including DE long non-coding RNAs (DElncRNAs) and DE microRNAs (DEmiRNAs) in NFPAs compared with normal samples. Then, we have assessed the relation between these genes and important signaling pathways. Our analyses led to identification of 3131 DEGs, including 189 downregulated DEGs (such as RPS4Y1 and DDX3Y) and 2898 upregulated DEGs (such as ASB3 and DRD4), and 44 DElncRNAs, including 8 downregulated DElncRNAs (such as NUTM2B-AS1 and MALAT1) and 36 upregulated DElncRNAs (such as BCAR4 and SRD5A3-AS1). GnRH signaling pathway, Tight junction, Gap junction, Melanogenesis, DNA replication, Nucleotide excision repair, Mismatch repair and N-Glycan biosynthesis have been among dysregulated pathways in NFPAs. Taken together, our study has revealed differential expression of several genes and signaling pathways in this type of tumors.
Long Intergenic Non-Protein Coding RNA 511 (LINC00511) is an RNA gene being mostly associated with lung cancer. Further assessments have shown dysregulation of this lncRNA in a variety of cancers. LINC00511 has interactions with hsa-miR-29b-3p, hsa-miR-765, hsa-mir-150, miR-1231, TFAP2A-AS2, hsa-miR-185-3p, hsa-miR-29b-1-5p, hsa-miR-29c-3p, RAD51-AS1 and EZH2. A number of transcription factors have been identified that regulate expression of LINC00511. The current narrative review summarizes the role of LINC00511 in different cancers with an especial focus on its prognostic impact in human cancers.
The construction of a competing endogenous RNA (ceRNA) network is an important step in the identification of the role of differentially expressed genes in cancers. In the current research, we used a number of bioinformatics tools to construct the ceRNA network in prostate cancer and identify the importance of these modules in predicting the survival of patients with this type of cancer. An assessment of microarray data of prostate cancer and normal samples using the Limma package led to the identification of differential expressed (DE) RNAs that we stratified into mRNA, lncRNA, and miRNAs, resulting in 684 DEmRNAs, including 437 downregulated DEmRNAs (such as TGM4 and SCGB1A1) and 241 upregulated DEmRNAs (such as TDRD1 and CRISP3); 6 DElncRNAs, including 1 downregulated DElncRNA (H19) and 5 upregulated DElncRNAs (such as PCA3 and PCGEM1); and 59 DEmiRNAs, including 30 downregulated DEmiRNAs (such as hsa-miR-1274a and hsa-miR-1274b) and 29 upregulated DEmiRNAs (such as hsa-miR-1268 and hsa-miR-1207-5p). The ceRNA network contained a total of 5 miRNAs, 5 lncRNAs, and 17 mRNAs. We identified hsa-miR-17, hsa-miR-93, hsa-miR-150, hsa-miR-25, PART1, hsa-miR-125b, PCA3, H19, RND3, and ITGB8 as the 10 hub genes in the ceRNA network. According to the ROC analysis, the expression levels of 19 hub genes showed a high diagnostic value. Taken together, we introduce a number of novel promising diagnostic biomarkers for prostate cancer.
Long non‐coding RNAs (lncRNAs) have been shown to be dysregulated in a variety of malignant and non‐malignant lesions including non‐functioning pituitary adenomas (NFPAs). In the current experimental study, we have selected six lncRNAs, namely MAPKAPK5‐AS1, NUTM2B‐AS1, ST7‐AS1, LIFR‐AS1, PXN‐AS1 and URB1‐AS1 to assess their expression in a cohort of Iranian patients with NFPA. MAPKAPK5‐AS1, PXN‐AS1 and URB1‐AS1 were shown to be over‐expressed in NFPA tissues compared with control samples (Expression ratios (95% CI) = 10 (3.94–25.36), 11.22 (4.3–28.8) and 9.33 (4.12–21.12); p values < 0.0001, respectively). The depicted ROC curves showed the AUC values of 0.73, 0.80 and 0.73 for MAPKAPK5‐AS1, PXN‐AS1 and URB1‐AS1, respectively. Relative expression level of PXN‐AS1 was associated with tumour subtype (p value = 0.49). Besides, relative expression levels of MAPKAPK5‐AS1 and LIFR‐AS1 were associated with gender of patients (p values = 0.043 and 0.01, respectively). Cumulatively, the current study indicates the possible role of MAPKAPK5‐AS1, PXN‐AS1 and URB1‐AS1 lncRNAs in the pathogenesis of NFPAs.
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