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Effect of Sprouty2 Downregulation on MicroRNA Expression Profile in HCT116 Colon Cancer Cells

ABSTRACT: Sprouty proteins are evolutionarily conserved modulators of mitogen-activated protein kinase pathway. Sprouty2 appears to function as a tumor suppressor in cancers, whereas we reported earlier that Sprouty2 functions as an oncogene in colorectal cancer. To further understand the oncogenic potential of Sprouty2 in the colon, microRNA expression profile of colon cancer cells was investigated. Sprouty2 suppression in HCT116 colon cancer cells significantly increased MicroRNA 194-5p. Sprouty2 dependent regulation of microRNA194-5p and its biological targets were studied further for their tumor suppressive actions in reducing epithelial-mesenchymal transition in colorectal cancer.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69665 | GEO | 2015/06/09

SECONDARY ACCESSION(S): PRJNA286128

REPOSITORIES: GEO

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Effect of Sprouty2 Downregulation on MicroRNA Expression Profile in HCT116 Colon Cancer Cells

Project description:Sprouty proteins are evolutionarily conserved modulators of mitogen-activated protein kinase pathway. Sprouty2 appears to function as a tumor suppressor in cancers, whereas we reported earlier that Sprouty2 functions as an oncogene in colorectal cancer. To further understand the oncogenic potential of Sprouty2 in the colon, microRNA expression profile of colon cancer cells was investigated. Sprouty2 suppression in HCT116 colon cancer cells significantly increased MicroRNA 194-5p. Sprouty2 dependent regulation of microRNA194-5p and its biological targets were studied further for their tumor suppressive actions in reducing epithelial-mesenchymal transition in colorectal cancer. Sprouty2 knockdown was performed by infecting HCT116 cells with three different lentivirus expressing shRNAs against human Sprouty2 mRNA and a control non targeted non-silencing shRNA (Sprouty2 MISSION shRNA Lentiviral Transduction Particles; TRCN 0000007522, TRCN 0000231589, TRCN 0000231588 and a non-targeted shRNA control from Sigma) following lentiviral transduction protocols provided by Sigma. Due to the random integration of the lentivirus into the host genome, varying levels of Sprouty2 gene knockdown was expected in puromycin resistant colonies. Three colonies in triplicate that demonstrated highest to lowest level of Sprouty2 suppression, as assessed by western blotting, were selected. RNA samples from these colonies and one from non-targeted shRNA expressing colony were prepared for microRNA expression profile analysis. Pooled RNA samples from each group were shipped to Exiqon for microRNA profiling based on miRCURY LNATM array technology.

2015-06-09 | E-GEOD-69665 | biostudies-arrayexpress

SPROUTY2 target genes in human colon carcinoma cells

2016-08-01 | GSE56941 | GEO

SPROUTY2 target genes in human colon carcinoma cells

Project description:The role of SPROUTY2 (SPRY2) in human colon cancer is controversial. Our data support a tumorigenic action of SPRY2. We use microarrays to identify SPRY2 target genes in human SW480 ADH colon carcinoma cell line. RNA was obtained from SW480 ADH cells, Mock transfected or transfected with WT or two differents SPRY2 genes mutants. Hybridization was performed on Affymetrix microarrays. We performed three independent experiments. Each experiment was conducted in triplicate.

2016-08-01 | E-GEOD-56941 | biostudies-arrayexpress

RNA-Seq of distal colonic homogenates from intestinal epithelial-specific Sprouty2-deleted mice versus littermate controls

Project description:We asked whether Sprouty2 controls secretory cell differentiation in the distal colon. Loss of Sprouty2 leads to expansion of tuft and goblet cell populations. Sprouty2 loss induced PI3K/Akt signaling, leading to GSK3β inhibition and epithelial IL-33 expression

2020-11-14 | GSE160854 | GEO

Downregulation of miR-194-5p induces paclitaxel resistance in ovarian cancer cells by altering MDM2 expression.

Project description:Paclitaxel is a first-line drug for treating epithelial ovarian cancer (EOC). However, prognosis for patients with advanced stage cancer remains poor due to primary or acquired drug resistance. Therefore, overcoming chemoresistance is one of the greatest challenges in treating EOC. In this study, we identified microRNAs (miRNA) that regulate paclitaxel resistance and tested their potential utility as therapeutic targets. Paclitaxel-resistant cell lines were established using two EOC cell lines: SKVO3ip1 and HeyA8. miRNA PCR arrays showed that miR-194-5p was downregulated in paclitaxel-resistant cells. Forced expression of miR-194-5p resensitized resistant cells to paclitaxel. Conversely, miR-194-5p inhibition induced paclitaxel resistance in parental cells. In silico analysis and luciferase reporter assay revealed that MDM2 is a direct target of miR-194-5p. MDM2 was upregulated in paclitaxel resistant cells compared with parental cells. MDM2 inhibition also resensitized resistant cells to paclitaxel and forced MDM2 induced paclitaxel resistance in parental cells. miR-194-5p induced p21 upregulation and G1 phase arrest in resistant cells by downregulating MDM2. Furthermore, a public database showed that high MDM2 expression was associated with a shorter progression-free survival in EOC patients treated with paclitaxel. Collectively, our results show that restoring miR-194-5p expression resensitizes EOCs to paclitaxel, and this may be exploited as a therapeutic option.

2019-10-18 | GSE139043 | GEO

Single cell RNA seq of colonic tissue from intestinal epithelial-specific Sprouty2-deleted mice and controls

Project description:In this study we asked how loss of Sprouty2 remodels colonic tissue and function. We show that loss of Sprouty2 promotes IL-13 signaling to regulate colonic secretory cells and furthermore identify deep crypt secretory cells as a reservoir for the host defense peptide RELMbeta.

2022-11-27 | GSE196803 | GEO

U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with MS275 (SNDX 275;Entinostat)

Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with MS275 (SNDX 275;Entinostat) for 24 h at 5uM concetration

2017-05-22 | GSE73647 | GEO

U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid)

Project description:Transcriptional profiling of U937 miR-194-5p (UmiR-194-5p) vs U937 miR-194-5p (UmiR-194-5p) treated with SAHA (Vorinostat; suberoylanilide hydroxamic acid) for 24 h at 5uM concetration

2017-05-22 | GSE73648 | GEO

Lysine tRNA fragments and miR-194-5p co-regulate hepatic steatosis via β-Klotho and Perilipin 2 (RNA)

Project description:Non-alcoholic fatty liver disease (NAFLD) involves hepatic accumulation of intracellular lipid droplets via incompletely understood processes. Here, we report distinct and cooperative NAFLD roles of LysTTT-5’tRF transfer RNA fragments and microRNA miR-194-5p. Unlike lean animals, dietary-induced NAFLD mice showed concurrent hepatic decrease of both LysTTT-5’tRF and miR-194-5p levels, which were restored following miR-132 antisense oligonucleotide treatment which suppresses hepatic steatosis. Moreover, exposing human-derived Hep G2 cells to oleic acid for 7 days co-suppressed miR-194-5p and LysTTT-5’tRF levels while increasing lipid accumulation. Importantly, transfecting fattened cells with a synthetic LysTTT-5’tRF mimic elevated mRNA levels of the metabolic regulator β-Klotho while decreasing triglyceride amounts by 30% within 24 hours. In contradistinction, antisense suppression of miR-194-5p induced accumulation of its novel target, the NAFLD-implicated lipid droplet-coating PLIN2 protein. Further, two out of 15 steatosis-alleviating screened drug-repurposing compounds, Danazol and Latanoprost, elevated miR-194-5p or LysTTT-5’tRF levels. The different yet complementary roles of miR-194-5p and LysTTT-5’tRF offer new insights into the complex roles of small non-coding RNAs and the multiple pathways involved in NAFLD pathogenesis.

2024-01-31 | GSE248320 | GEO

Lysine tRNA fragments and miR-194-5p co-regulate hepatic steatosis via β-Klotho and Perilipin 2 (small RNA II)

2024-01-31 | GSE248319 | GEO

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