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MicroRNA?363?3p inhibits hepatocarcinogenesis by targeting HMGA2 and is associated with liver cancer stage.

ABSTRACT: The importance of microRNAs (miRNAs) in cancer development has been widely recognized in recent decades. In the present study, the function and mechanism of miRNA?363?3p (miR?363?3p), formerly characterized as a tumor suppressor, in the hepatocarcinogenesis of liver cancer cells was investigated. Reverse transcription?quantitative polymerase chain reaction (RT?qPCR) was applied to detect the expression of miR?363?3p in liver cancer tissues. Cell proliferation, survival and migration capacities were determined by MTT, colony formation and wound?healing assays, respectively. The targeting of high mobility group AT?hook 2 (HMGA2) mRNA by miR?363?3p was confirmed by bioinformatics analysis, and RT?qPCR, luciferase reporter and western blot assays. The correlation between the expression levels of HMGA2 and miR?363?3p was analyzed. The RT?qPCR results revealed that the levels of miR?363?3p were downregulated in liver cancer tissues. Cellular assays validated that miR?363?3p exerted tumor suppressing functions, including the inhibition of cell proliferation, survival and migration abilities in two liver cancer cell lines. Bioinformatics prediction and subsequent experiments demonstrated that HMGA2 was a direct target of miR?363?3p. Restoration of the expression of HMGA2 in miR?363?3p mimic?transfected cells reversed the tumor suppressing effects caused by miR?363?3p. Finally, there was a significant negative correlation between the expression levels of HMGA2 and miR?363?3p in liver cancer tissues. miR?363?3p was identified as an important tumor suppressor in liver cancer via targeting HMGA2, which may have potential benefits in liver cancer therapy.

SUBMITTER: Wang J

PROVIDER: S-EPMC6323225 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature

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MicroRNA‑363‑3p inhibits hepatocarcinogenesis by targeting HMGA2 and is associated with liver cancer stage.

Wang Jing J Liang Huimin H Ge Haize H Guo Xinling X Gu Dongmei D Yuan Yuhua Y

Molecular medicine reports 20181129 2

The importance of microRNAs (miRNAs) in cancer development has been widely recognized in recent decades. In the present study, the function and mechanism of miRNA‑363‑3p (miR‑363‑3p), formerly characterized as a tumor suppressor, in the hepatocarcinogenesis of liver cancer cells was investigated. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was applied to detect the expression of miR‑363‑3p in liver cancer tissues. Cell proliferation, survival and migration capacities w ...[more]

PMID: 30535489

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Project description:BackgroundRunt-related transcription factor 1 (RUNX1) is one of the most frequently mutated genes in most of hematological malignancies, especially in acute myeloid leukemia. In the present study, we aimed to identify the key genes and microRNAs based on acute myeloid leukemia with RUNX1 mutation. The newly finding targeted genes and microRNA associated with RUNX1 may benefit to the clinical treatment in acute myeloid leukemia.Material/methodsThe gene and miRNA expression data sets relating to RUNX1 mutation and wild-type adult acute myeloid leukemia (AML) patients were downloaded from The Cancer Genome Atlas database. Differentially expressed miRNAs and differentially expressed genes (DEGs) were identified by edgeR of R platform. Gene ontology and the Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed by Metascape and Gene set enrichment analysis. The protein-protein interaction network and miRNA-mRNA regulatory network were performed by Search Tool for the Retrieval of Interacting Genes database and Cytoscape software.ResultsA total of 27 differentially expressed miRNAs (25 upregulated and 2 downregulated) and 561 DEGs (429 upregulated and 132 downregulated) were identified. Five miRNAs (miR-151b, miR-151a-5p, let-7a-2-3p, miR-363-3p, miR-20b-5p) had prognostic significance in AML. The gene ontology analysis showed that upregulated DEGs suggested significant enrichment in MHC class II protein complex, extracellular structure organization, blood vessel development, cell morphogenesis involved in differentiation, embryonic morphogenesis, regulation of cell adhesion, and so on. Similarly, the downregulated DEGs were mainly enriched in secretory granule lumen, extracellular structure organization. In the gene set enrichment analysis of Kyoto Encyclopedia of Genes and Genomes pathways, the RUNX1 mutation was associated with adherent junction, WNT signaling pathway, JAK-STAT signaling pathway, pathways in cancer, cell adhesion molecules CAMs, MAPK signaling pathway. Eleven genes (PPBP, APP, CCR5, HLA-DRB1, GNAI1, APLNR, P2RY14, C3AR1, HTR1F, CXCL12, GNG11) were simultaneously identified by hub gene analysis and module analysis. MicroRNA-363-3p may promote the development of RUNX1 mutation AML, targeting SPRYD4 and FNDC3B. In addition, the RUNX1 mutation rates in patient were obviously correlated with age, white blood cell, FAB type, risk(cyto), and risk(molecular) (P < .05).ConclusionOur findings have indicated that multiple genes and microRNAs may play a crucial role in RUNX1 mutation AML. MicroRNA-363-3p may promote the development of RUNX1 mutation AML by targeting SPRYD4 and FNDC3B.

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MicroRNA?363?3p inhibits hepatocarcinogenesis by targeting HMGA2 and is associated with liver cancer stage.

Publications

MicroRNA‑363‑3p inhibits hepatocarcinogenesis by targeting HMGA2 and is associated with liver cancer stage.

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