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

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

PROVIDER: PRJNA578133 | ENA |

REPOSITORIES: ENA

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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

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

Project description: Not available

| S-EPMC6363016 | biostudies-literature

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

U937 scramble (Usc) vs U937 miR-194-5p (UmiR-194-5p)

Project description:Transcriptional profiling of U937 scramble vs U937 miR-194-5p (UmiR-194-5p)

2017-05-22 | GSE73646 | GEO

Identification of miR-194-5p target genes in gastric cancer

Project description:Increasing studies report that miR-194-5p plays a tumor suppressor role in gastric cancer (GC). Previous studies have revealed that miR-194 inhibited gastric cancer progression through different pathways by affecting the expression level of different target genes. For example, miR-194 have been reported to be able to regulate the expression of FOXM1, NR2F2, BMI1, SDAD1, RBX1, KDM5B, ZEB1 and AKT2 etc. It suggested that miR-194 may play complicated roles in GC. To figure out the mechanism of miR-194' tumor suppressor role in GC, we performed RNA sequencing in two different GC cell lines. Our studies showed that miR-194 tends to regulated target genes by binding on their 3' untranslated regions with either 7-mer-A1 or 7-mer-m8 or 8-mer. Approximately 138 genes were downregulated in both SGC7901 and BGC823 cell lines that transfected with miR-194-5p mimics compared to negative control siRNAs. Most of the downregulated genes have not reported yet.

2019-10-01 | GSE134308 | GEO

Circulating miR 802-5p and miR 194-5p and brain expression of MEF2C as novel biomarkers of breast cancer brain metastasis

Project description:We hypothesized that circulating miRNAs could work as biomarkers for early detection of breast cancer brain metastasis (BCBM), and their targets could constitute new targets for modulation. We used a mouse model of BCBM and Next-Generation Sequencing to establish the circulating miRNAs alterations along brain metastasis development and performed bioinformatics analysis to identify their targets with relevance in the metastatic process. We additionally analyzed human resected brain metastasis of breast cancer patients for target’s expression validation. In our mouse model, we observed a deregulation of circulating miRNAs profile during BCBM progression, with a downregulation of miR-802-5p and miR-194-5p in plasma prior to brain metastases detection. The transcription factor myocyte enhancer factor 2C (MEF2C), was identified as a target for both miRNAs, and its expression was increasingly observed in malignant cells along brain metastasis development. Its upregulation was also observed in peritumoral astrocytes and in human BCBM. Collectively, downregulation of circulating miR-802-5p and miR-194-5p appear as precocious biomarkers for BCBM and MEF2C emerges as a new player and a potential target for modulation.

2019-12-02 | GSE136149 | GEO

miR-17-5p downregulation contributes to paclitaxel resistance of lung cancer cells through altering beclin1 expression.

Project description: Not available

| S-EPMC3995800 | biostudies-literature

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

The miR-194-5p/BCLAF1 module is responsible for maturation block, cell fate and treatment susceptibility in AML.

Project description:miRNAs deregulation contributes to cancer. miR-194-5p is up-regulated by the HDAC inhibitor (HDACi) SAHA, negatively modulating BCL2-associated transcription factor 1 (BCLAF1). We prove that the miR-194-5p/BCLAF1 equilibrium regulates differentiation, survival and self-renewal of normal progenitors and acute myeloid leukemia (AML) blasts. This equilibrium is perturbed in AMLs resulting in highly expressed BCLAF1, suppression of miR194-5p, consequently, locking cells into an immature, potentially ‘immortal’ state. HDACis reverse this scenario relocating BCLAF1 from the nucleus to a peri-membrane ring-like cytoplasmic structure, sensitizing the cells to differentiation or apoptosis. miR-194-5p and BCLAF1 are significantly deregulated in a cohort of 60 primary AMLs and get restored by HDACi. Our findings connect responsiveness to treatment to re-instatement of miR-194-5p/BCLAF1 balance. These findings might be exploited for (epi-based) anti-leukemia therapy.

2017-12-20 | GSE76426 | GEO

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