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Microarray Analysis of MKN-45 cell lines after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.

ABSTRACT: We demonstrate that miR-125b, a key node in this microRNA regulatory network, is upregulated in gastric cancer (GC) and associated with poor overall survival through an integrated analysis of microRNA and mRNA profiling of GC revealed a mRNA-regulatory network.So we have employed whole genome microarray expression profiling as a discovery platform to compare the transcriptome profiling of human gastric cells (MKN-45) after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.Pathway analysis shows that the predicted targets of miR-125b are highly involved in apoptosis/program death pathway，and the robust apoptosis genes, BIK and CASP6 are validated as the directed targets of miR-125b.

ORGANISM(S): Homo sapiens

PROVIDER: GSE145959 | GEO | 2021/02/25

REPOSITORIES: GEO

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microarray Analysis of MKN-45 cell lines after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.

Project description:microarray Analysis of MKN-45 cell lines after 48 hours post-transfection of miR-125b mimic (50nM) and mimic control.

| PRJNA608875 | ENA

mRNA profiling of white hMADS cells converted in brite adipocytes and transfected with mimic miR-125b-5p

Project description:miR-125b-5p is a well known miRNA already describded in several forms of cancer. miR-125b-5p is expressed in adipose tissue, adipocytes as well as their precursor cells. We aim to invest the role of miR-125b-5p in white adipocytes conversion into brite adipocytes. To get an idea about putative targets of miR-125b-5p in adipocyte conversion, we transfected miR-125b-5p mimic in human Multipotent Adipose-Derived Stem (hMADS) cells, differenciated in white adipocytes. Gene expression profiling is performed 48h after hMADSC transfection. Two-condition experiment, hMADS cells at day 16 after conversion of white adipocytes into brite adipocytes, comparison of cells transfected with a mimic miR-125b-5p to cells transfected with a negative controle. Biological replicates: 4, indepently grown and harvested. On each array, one biological replicate of mimic miR-125b-5p transfected cells was directly compared to one biological replicate of mimic negative control transfected cells (serving as reference sample). All hybridizations were repeated with reversed dye assignment (dye-swap) as technical replicates.

2016-07-01 | E-GEOD-80816 | biostudies-arrayexpress

mRNA profiling of white hMADS cells converted in brite adipocytes and transfected with mimic miR-125b-5p

2016-07-01 | GSE80816 | GEO

miR-125b controls mitochondrial metabolism and dynamics by targeting BIK and MTP18

Project description:Abnormal mitochondria metabolism and innate immune responses participate in the pathogenesis of many inflammatory disorders. The molecular events regulating mitochondrial activity to control survival and cell death in monocytes/macrophages are poorly understood. Here we show that miR-125b attenuates the activity of the mitochondrial respiratory chain through BIK silencing, and promotes the elongation of mitochondrial network through MTP18 targeting, without impacting autophagy, in the human monocytes. Proinflammatory activation is associated with a concomitant increase in miR-125b expression, decrease in BIK and MTP-18 expression, reduced oxidative phosphorylation, and enhanced mitochondrial fusion. Furthermore, expression of M1-associated transcripts as well as mitochondrial dynamics and energy metabolism are induced upon ectopic expression of miR-125b. In turn, by repressing miR-125b, mitochondrial dynamics was preserved, LPS-induced repression of BIK expression and of mitochondrial respiration were prevented, and M1 polarization of macrophages was inhibited. Altogether, our data reveal a novel role for miR-125b in controlling mitochondrial metabolism and dynamics by targeting BIK and MTP18, respectively, two novel cellular target proteins involved in maintaining the mitochondrial integrity in human monocytes. These findings not only suggest a novel function for miR-125b in regulating metabolic adaptation of monocytes to inflammation but also unravel new molecular mechanisms for its pro-apoptotic role and identify potential targets for interfering with inflammatory activation of monocytes.

2016-10-06 | GSE62693 | GEO

Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [RNA-seq]

Project description:To investigate the role of Fusobacterium nucleatum (Fn) in the development of gastric cancer, we extracted exosomes from the culture supernatant of MKN-28 cells treated with Fn or PBS, co-cultured them with AGS cells, and analyzed their RNA-seq data for gene expression profiling.

2023-06-07 | GSE214817 | GEO

Gastric cancer cells treated with exosomes derived from Fusobacterium nucleatum infected MKN-28 cells [miRNA-seq]

2023-06-07 | GSE213833 | GEO

miR-125b-EPO

Project description:MiR-125b possible targets were identified after transfecting a miRNA-mimic (miR-125b) and a scramble miRNA (Negative control) in MCF7 cell line and analyzing gene expression modifications.

2013-12-02 | E-MTAB-1604 | biostudies-arrayexpress

Effect of miR-125b and its isomiRs on gene expression subjected to hypoxic challenge

Project description:To investigate the gene expresiion regulated by miR-125b and its isomiRs. We transfected H9C2 cells with respective mimics and performed gene expression profiling anlaysis using data from RNA-seq of mimic controls, miR-125b and its isomiRs mimics subjected to normoxia and hypoxia treatment.

2023-11-22 | GSE227958 | GEO

Examination of HMGA2 binding genes in human HMGA2-exogenous overexpressed gastric cancer cells

Project description:HMGA2 significantly increased cell proliferation capacity of gastric cancer in a HMGA2-dependent manner both in vivo and in vitro and we found HMGA2 promoted GC through accelerating S-G2/M phase.To elucidate the underlining mechanism by which HMGA2 induced the change of phenotype in GC cells, we performed ChIP-seq analysis of HMGA2-OE MKN-45 cells with anti-HMGA2 antibody.

2021-08-18 | GSE174442 | GEO

Development of microRNA expression signatures for gastric cancer

Project description:To further investigate of microRNA expression profile of gastric cancer, we have employed whole microRNA gene chip as a discovery platform to identify gene differential expression between gastric cancer tissues with mormal gastric tissues.Expression of four microRNAs (miR-125b,miR-451,miR-192b,miR-200b) from this signature was quantified and verified in the same RNA samples by real-time PCR.

2011-01-15 | GSE26645 | GEO

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