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MicroRNA expression changes after knocking out MYEOV in two human pancreatic cancer cell lines

ABSTRACT: Pancreatic cancer (PC) remains a highly lethal malignancy worldwide. As metastasis and malignant proliferation are primarily responsible for poor clinical outcomes of PC, it is imminent to dig out the pivotal gene involved in the process as well as its underlying molecular mechanism. In this study, through analysis of TCGA and GTEx data, we found that the expression level of MYEOV was obviously increased in carcinoma tissues relative to healthy ones and associated with poor survival in PC patients. The elevated abundance of MYEOV was positively correlated with enhanced cell proliferation, invasion and migration in vivo and in vitro. The global transcriptome analysis of MYEOV-depleted PC cells revealed the downregulation of various genes involved in active cell proliferation, which indicated that MYEOV overexpression was critical for PC progression. MiRNA-seq analysis showed that MYEOV had a regulatory effect on the expression levels of miR-17-5p and miR-93-5p, depletion of which resulted in reduced cell proliferation, invasion and migration as observed in MYEOV-knockdown PC cells. Such effect was imposed by MYEOV through affecting enrichment of the transcription factor c-myc at the gene promoter regions of the two miRNAs. Furthermore, a complex containing MYEOV and MYC was confirmed to exist in cell nucleus, providing convictive evidence for the association of MYEOV with MYC. Together, these results suggested that the axis of MYEOV-MYC-miR-17/93-5p could be vital for PC progression and could act as a potential therapeutic target to interrupt cell proliferation which will benefit treatment and management of PC patients.

ORGANISM(S): Homo sapiens

PROVIDER: GSE143828 | GEO | 2021/12/29

REPOSITORIES: GEO

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Project description:Sepsis remains a leading cause of death and currently has no pathogenesis-specific therapy. Hampered progress is partly due to the lack of insight into deep mechanistic processes. Deciphering the functions of microRNAs in sepsis pathogeny became a dynamic research topic in the last decade. To screen for new microRNA targets for sepsis therapeutics, we used human samples: microRNA array data from peripheral blood mononuclear cells (PBMCs) from sepsis patients and controls, whole blood samples from sepsis survivors; and multiple animal models: mouse cecum ligation-puncture (CLP)-induced sepsis, mouse viral microRNA challenge, and baboon Gram-positive and Gram-negative sepsis models. miR-93-5p met the criteria for a therapeutic target, being overexpressed in baboons which died early after induction of sepsis and downregulated in humans who survived after sepsis. Therapeutically, inhibiting miR-93-5p prolonged the overall survival of mice with CLP-induced sepsis, with a stronger effect in old mice. Mechanistically, anti-miR-93-5p therapy reduced inflammatory monocytes and increased circulating effector memory T cells, especially CD4+ subset. Ago2-immunoprecipitation in miR-93-knockout T cells identified important regulatory receptors, CD28 and CD160, as direct miR-93-5p target genes. In conclusion, miR-93-5p is a potential therapeutic target in sepsis in the elderly through its regulation of both innate and adaptive immunity. We applied the Ago2-RIP Chip (Ribonucleoprotein ImmunoPrecipitation followed by microarray analysis) to identify miR-93-5p target mRNAs. This methodology uses beads coupled to either anti-Ago2 antibody (or an IgG control) to pull down the RISC complex together with any miRNA-interacting mRNAs. To define target genes of miR-93-5p, we assessed mRNA transcripts enriched in the Ago2-IP fraction of JURKAT parental cells or control cells (where miR-93-5p is present) but not in the two KO clones (where miR-93-5p is absent) by microarray

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MicroRNA expression changes after knocking out MYEOV in two human pancreatic cancer cell lines

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