Identification of eight key miRNAs associated with renal cell carcinoma: A meta‑analysis

Abstract

Renal cell carcinoma (RCC) is the most common renal carcinoma in the human kidney. To date, to the best of our knowledge, there are no biomarkers for the early monitoring and diagnosis of RCC patients. The present study aimed to develop deeper insight into the molecular mechanisms of microRNAs (miRNAs/miRs) in the regulation of RCC development and to reveal candidate miRNA biomarkers in human RCC. A meta-analysis was used to integrate the published and independent RCC miRNA expression profiling investigations that compared the miRNA expression profiles in RCC samples with control samples. The meta-signature miRNA target genes were then predicted in TargetScan. The predicted targets were further analyzed using Gene Ontology and pathway enrichment analysis with the Database for Annotation, Visualization and Integrated Discovery online tool, and then the transcription factors of meta-signature miRNA target genes were identified in Tfacts. A total of 7 publicly available and independent RCC miRNA expression profiling datasets were collected, and 2 upregulated (hsa-miR-155-5p and hsa-miR-210-5p) and 6 downregulated (hsa-miR-138-5p, hsa-miR-141-5p, hsa-miR-200c-5p, hsa-miR-362-5p, hsa-miR-363-5p and hsa-miR-429) meta-signature miRNAs in renal carcinoma were identified. The targeted gene enrichment analysis indicated that the meta-signature miRNAs may influence several pathways that participate in cancerogenesis, including the ‘rap1 signaling pathway’, ‘renal cell carcinoma’ and ‘microRNAs in cancer’. Overall, the present meta-analysis identified 2 upregulated and 6 downregulated meta-signature miRNAs from 7 renal carcinoma datasets, the dysregulated miRNAs that may contribute to kidney carcinoma development. This research may reveal candidate miRNA biomarkers in human RCC.

MiR-362-5p, Which Is Regulated by Long Non-Coding RNA MBNL1-AS1, Promotes the Cell Proliferation and Tumor Growth of Bladder Cancer by Targeting QKI

“…Increasing numbers of studies indicate that miR-362-5p promotes cell proliferation, tumor growth, and metastasis in hepatocellular carcinoma, human breast cancer, and lung cancer (Ni et al, 2015;Ni et al, 2016;Luo et al, 2018). However, miR-362-5p inhibits proliferation and migration of neuroblastoma cells and it is downregulated in renal cell carcinoma (Wu et al, 2015;Ying et al, 2018). It indicates that miR-362-5p could play oncogenic or suppressive roles in progression of these cancers.…”

Immunomodulatory MicroRNAs in cancer: targeting immune checkpoints and the tumor microenvironment

“…Another inhibitor for PD-L1 expression is miR-138-5p, which can be considered as a tumor suppressor that is commonly deficient in colorectal cancer (CRC) and linked to poor clinical outcomes [18]. miR-138-5p was recently identified as one of the key miR-NAs dysregulated in renal cell carcinoma (RCC) [21]. The expression of miR-138 is also reduced in squamous cell carcinoma of the head and neck, thyroid, and ovarian tumors [19,20].…”

“…The expression of miR-138 is also reduced in squamous cell carcinoma of the head and neck, thyroid, and ovarian tumors [19,20]. miR-138-5p was recently identified as one of the key miR-NAs dysregulated in renal cell carcinoma (RCC) [21]. miR-138-5p mimics were shown to inhibit the cell proliferation and invasion of RCC cell lines [22].…”

Cell proliferation is induced in renal cell carcinoma through miR‑92a‑3p upregulation by targeting FBXW7

“…MicroRNAs (miRNAs) are small non-coding RNAs (~22 nucleotides in length) that regulate gene expression on a post-transcriptional level through base-pairing with complementary sequences of the 3'untranslated region (UTR) of mRNAs (8). Recent studies demonstrated that miR-720 and eight other miRNAs serve crucial roles in RCC (9,10). For example, miR-92a-3p has been reported to serve a crucial role in the progression of various types of cancer, including lung cancer, esophageal squamous cell carcinoma, colorectal, breast, ovarian, and cervical cancer (11)(12)(13)(14)(15)(16).…”