Dataset Information

Downregulation of miR?136?5p in hepatocellular carcinoma and its clinicopathological significance.

ABSTRACT: The clinical significance of microRNA (miR)?136?5p in hepatocellular carcinoma (HCC) has not been verified. Therefore, in the current study, the authors aimed to explore miR?136?5p expression and its clinical significance in HCC, as well as to investigate its potential target genes function. The authors detected the levels of miR?136?5p in 101 pairs of HCC and para?cancer tissues via reverse transcription?quantitative polymerase chain reaction. Gene Expression Omnibus database and the Cancer Genome Atlas (TCGA) database were used to further verify the clinical significance of miR?136?5p expression in HCC. The target genes prediction analysis of miR?136?5p, natural language processing (NLP) analysis of HCC in PubMed and gene functional enrichment analysis were conducted. The miR?136?5p level was markedly downregulated in HCC tissue, compared to para?non?tumor tissue. MiR?136?5p expression decreased in HCC patients with metastasis (P=0.004), advance TNM stage (P<0.001), portal vein tumor embolus (P=0.007) and vaso?invasion (P=0.003), compared with those HCC patients with non?metastasis, early TNM stage, non?portal vein tumor embolus and non?vaso?invasion, respectively. In the TCGA database, downregulated miR?136?5p was also observed in HCC tissue compared to normal liver tissue (P<0.001). There were 178 genes obtained from the overlap between predicted targets and NLP analysis. GO and KEGG pathway analyses revealed some significant pathways related to cancers. Downregulation of miR?136?5p may be responsible for the carcinogenesis and aggressiveness of HCC. miR?136?5p may act as an anti?carcinoma miRNA, which is essential for HCC progression through the regulation of various signaling pathways. Thus, miR?136?5p interaction may provide a novel strategy for HCC treatment.

SUBMITTER: Ding H

PROVIDER: S-EPMC5647073 | biostudies-literature | 2017 Oct

REPOSITORIES: biostudies-literature

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Downregulation of miR‑136‑5p in hepatocellular carcinoma and its clinicopathological significance.

Ding Hua H Ye Zhi-Hua ZH Wen Dong-Yue DY Huang Xiao-Liang XL Zeng Chu-Mei CM Mo Jie J Jiang Yi-Qiang YQ Li Jian-Jun JJ Cai Xiao-Yong XY Yang Hong H Chen Gang G

Molecular medicine reports 20170817 4

The clinical significance of microRNA (miR)‑136‑5p in hepatocellular carcinoma (HCC) has not been verified. Therefore, in the current study, the authors aimed to explore miR‑136‑5p expression and its clinical significance in HCC, as well as to investigate its potential target genes function. The authors detected the levels of miR‑136‑5p in 101 pairs of HCC and para‑cancer tissues via reverse transcription‑quantitative polymerase chain reaction. Gene Expression Omnibus database and the Cancer Gen ...[more]

PMID: 28849100

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Project description:Decreased level of miR-204-5p has been documented in various malignancies. However, the expression and clinical significance of miR-204-5p in hepatocellular carcinoma has not been investigated. The aim of this study is to examine the relationship between miR-204-5p expression and clinicopathological features in hepatocellular carcinoma (HCC) as well as to predict the relevant signaling pathways. The miR-204-5p expression level was detected in HCC and in matched paraneoplastic liver from 95 formalin-fixed paraffin-embedded tissues by the real-time reverse transcription polymerized chain reaction (qRT-PCR). The association of miR-204-5p expression with clinicopathological features as well as the prognosis of HCC was examined. Public data portals including the Gene Expression Omnibus and The Cancer Genome Atlas were used to retrieve the HCC-related data in order to perform a comprehensive meta-analysis. Meanwhile, protein-protein interaction (PPI) and enrichment analyses were performed using predicted target genes. The relative expression of miR-204-5p was remarkably reduced in HCC than that in paraneoplastic hepatic tissues. In HCC, the miR-204-5p expression was downregulated in the metastasis, vasoinvasion, and advanced stage (III and IV) subgroups compared with their counterparts. Furthermore, the meta-analysis based on qRT-PCR data demonstrated that miR-204-5p was markedly downregulated in HCC with a standardized mean difference of -5.19 (P?<?.001). However, no significant association was observed between miR-204-5p and survival outcomes. The potential target genes of miR-204-5p were significantly enriched in several pathways which might be associated with HCC, such as "cell proliferation" from GO terms and "pathways in cancer" from the KEGG analysis. A PPI network of miR-204-5p potential target genes identified prospective core genes potentially involved in the regulation of HCC oncogenesis and progression. Our findings suggested that miR-204-5p might act as a tumor-suppressive gene in the tumorigenesis and progression of HCC via vital signaling pathways and that miR-204-5p could be regarded as a protective factor in HCC.

Project description:BackgroundThe clinical significance of miR-141-3p in hepatocellular carcinoma has not been verified. Therefore, we conducted this study to examine miR-141-3p expression and its clinical significance in hepatocellular carcinoma and to investigate the functions of its potential targets.MethodsThe Cancer Genome Atlas database and the Gene Expression Omnibus database were used to explore the aberrant expression of miR-141-3p in hepatocellular carcinoma. Furthermore, we assessed the miR-141-3p levels in 95 hepatocellular carcinoma tissues with 95 matched adjacent tissues using real-time quantitative polymerase chain reaction. Moreover, a target gene prediction analysis of miR-141-3p, a natural language processing analysis for hepatocellular carcinoma using PubMed, and a gene functional enrichment analysis were conducted to search the potential function of miR-141-3p in the pathogenesis of hepatocellular carcinoma.ResultsRegarding The Cancer Genome Atlas data, miR-141-3p levels were markedly downregulated in hepatocellular carcinoma tissue compared to para- or nontumor tissue (4.6112 [1.7096] vs 5.3053 [1.4254], P = .045). MiR-141-3p expression was reduced in patients with hepatocellular carcinoma with a low pathologic T stage (P = .006), a low grade (P = .01), elderly hepatocellular carcinoma patients (P = .001), and male patients with hepatocellular carcinoma (P = .01) compared with that in patients with hepatocellular carcinoma with high pathologic T stages, high grades, young patients with hepatocellular carcinoma, and female patients with hepatocellular carcinoma. However, according to the Gene Expression Omnibus database, no significant differences in the expression of miR-141-3p were observed between hepatocellular carcinoma tissue and normal liver tissue (P = .984). Real-time quantitative polymerase chain reaction confirmed a similar trend of decreased miR-141-3p in hepatocellular carcinoma tissue (1.7542 [0.8663] vs 2.5562 [1.7913], P = .001) as observed in The Cancer Genome Atlas. In addition, decreased miR-141-3p levels were detected in the multiple tumor nodes group (P = .004), the metastasis group (P < .001), and the advanced TNM stage group (P = .01), compared to the single tumor nodes group, the nonmetastasis group, and the early TNM stage group. Two hundred eighty-two genes were identified from the overlap between the predicted targets and the natural language processing analysis. Gene ontology and Kyoto Encyclopedia of Genes and Genomes pathway analyses revealed several significant biological functions and pathways related to the pathogenesis of cancers, including hepatocellular carcinoma.ConclusionDownregulation of miR-141-3p might be responsible for the carcinogenesis and aggressiveness of hepatocellular carcinoma. MiR-141-3p may act as an antitumor microRNA, which is essential for hepatocellular carcinoma progression through the regulation of various signaling pathways. Thus, interactions with miR-141-3p may provide a novel strategy for hepatocellular carcinoma treatment in the future.

Project description:BACKGROUND:Thyroid carcinoma (TC) is a common malignancy of the endocrine system. This research aimed to examine the expression levels of miR-136-5p and metadherin (MTDH) in TC and unveil their potential targeting relationship. METHODS:TC microRNA (miRNA) microarray and miRNA-sequencing data were collected to evaluated miR-136-5p expression. We assessed the comprehensive expression of miR-136-5p by calculating the standard mean difference (SMD) and summary receiver operating characteristic curves (sROC). Subsequently, the miR-136-5p mimic and inhibitor were transfected into the TC B-CPAP cell, Thiazolyl Blue Tetrazolium Bromide (MTT) assay and cell apoptosis assay by FACS with Annexin V-/7-AAD double staining were performed to explore the biological role of miR-136-5p in the B-CPAP cell line. Prediction of target genes and potential biological function analysis of miR-136-5p were made using miRWalk2.0 and DAVID, respectively. Through target gene prediction, MTDH may be the candidate target gene of miR-136-5p. Subsequently, gene microarrays and RNA-sequencing data were also leveraged for MTDH expression. The meta-analysis method was conducted to evaluate the comprehensive expression level of MTDH. In addition, MTDH protein expression was identified using immunohistochemistry. The MTDH protein levels post-miR-136-5p transfection were verified by western blot, and the dual luciferase reporter assay was adapted to confirm the direct targeting relation between miR-136-5p and MTDH. RESULTS:The miR-136-5p level was remarkably downregulated in TC, the pooled SMD was -0.47 (95% CI: -0.70 to -0.23, I2=36.6%, P=0.192) and the area under the curve (AUC) of the sROC was 0.67 based on 543 cases of TC. MTT indicated that the overexpression of miR-136-5p dramatically inhibited the proliferation of B-CPAP cells. The cell apoptosis increased in the miR-136-5p mimic group compared to the negative control group. In addition, both MTDH mRNA and protein levels were markedly overexpressed, with the pooled SMD being 0.94 (95% CI: -0.35 to 2.24, I2=98.8%, P<0.001), and the AUC of the sROC being 0.85 with 1054 cases of TC. The MTDH protein level was significantly up-regulated in TC than in the non-carcinomic tissues by immunohistochemistry (8.292±1.717 vs. 2.618±2.570, P<0.001). Western blot indicated that MTDH protein expression was suppressed by miR-136-5p mimic in the B-CPAP cell line, which was further supported by the dual luciferase reporter assay. CONCLUSION:The miR-136-5p/MTDH axis may play a vital role in modulating TC tumorigenesis, providing new insight into possible molecular mechanisms of TC oncogenesis.

Dataset Information

Downregulation of miR?136?5p in hepatocellular carcinoma and its clinicopathological significance.

Publications

Downregulation of miR‑136‑5p in hepatocellular carcinoma and its clinicopathological significance.

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