Dual Functional MicroRNA-186-5p Targets both FGF2 and RelA to Suppress Tumorigenesis of Glioblastoma Multiforme

Wang, Fachen; Jiang, Hui; Shan-jun, Wang; Chen, Bing

doi:10.1007/s10571-017-0474-4

Cited by 25 publications

(22 citation statements)

References 33 publications

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“…By targeting YAP1, miR-186 inhibited proliferation, migration, and invasion of pancreatic cancer (31) and hepatocellular carcinoma cells (32). Moreover, miR-186 repressed invasion and migration by directly targeting TBL1XR1 and FOXK1 in osteosarcoma cells (52,53), or targeting FGF2 and RelA in glioblastoma multiforme cells (43). MiR-186 inhibited proliferation of human pituitary tumor cells through targeting SKP2, thus upregulating p27 Kip1 expression, a well-known negative regulator of G1 cell cycle progression (44).…”

Section: Mir-186 As a Tumor Suppressor Mirnamentioning

confidence: 99%

The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA

et al. 2020

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MicroRNAs (miRNAs) are a class of small non-coding RNAs which regulate gene expression at post-transcriptional level. Alterations of miR-186 expression were demonstrated in numerous cancers, shown to play a vital role in oncogenesis, invasion, metastasis, apoptosis, and drug resistance. MiR-186 was documented as a tumor suppressor miRNA in the majority of studies, while conflicting reports verified miR-186 as an oncomir. The contradictory role in cancers may impede the application of miR-186, as well as other dual-functional miRNAs, as a diagnostic and therapeutic target. This review emphasizes the alterations and functions of miR-186 in cancers and discusses the mechanisms behind the contradictory findings. Among these, target abundance and dose-dependent effects of miR-186 are highlighted. The paper aims to review the challenges involved in developing diagnostic and therapeutic strategies for cancer treatment based on dual-functional miRNAs.

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Section: Mir-186 As a Tumor Suppressor Mirnamentioning

confidence: 99%

The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA

et al. 2020

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“…Remarkably, in human THP-1 macrophages miR-186 enhances secretion of IL-6, IL-1β and TNF-α as well as lipid accumulation via targeting cystathionine-γ-lyase ( CSE ) [217]. Moreover, in human glioblastoma cells FGF2 and the NF-κB subunit RelA have been identified as miR-186 targets [218]. Summarized, despite induction of inflammatory cytokine expression by miR-186, the inflammatory response is apparently attenuated via NF-κB depletion.…”

Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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“…A study demonstrated that RELA is a mediator of oncogene of pancreatic ductal adenocarcinoma, and the bene cial effects of RELA were mediated by increased expression of CXCL1 and CXCR2 23 . NFKB1 as a suppressor of the NF-κB response contributed to tumorigenesis in many types of cancer, including GBM 24 . The cumulative data demonstrated CXC chemokine and NF-κB pathway may become potentially molecular targets in the clinical treatment of GBM.…”

Section: Discussionmentioning

confidence: 99%

Identification of Prognostic Biomarkers and Immunotherapeutic Targets with CXC Chemokines in Glioblastoma Multiforme Using Integrated Bioinformatic Analysis

Liu¹,

Zhu²,

Wang³

2020

Preprint

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Background Glioblastoma multiforme (GBM) is the most malignant central nervous system tumour bearing a dismal prognosis. The study aimed to explore the potential biomarkers and therapeutic targets with CXC chemokines in GBM by integrated bioinformatics analysis.Methods Differentially expressed CXC Chemokines were identified in GBM using GEPIA and UALCAN databases,and Kaplan–Meier analyses were performed by GEPIA subsequently. Protein -protein interaction (PPI) network was established in STRING database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis were utilized to analyze differentially expressed CXC Chemokines and their similar genes gained from GEPIA. Then, we conducted transcription factors, kinase targets, and immune cells infiltration using TRRUST, LinkedOmics, and TIMER, respectively.Results The mRNA expression levels of CXCL3/5/6/9/10/11/12/13/16 in GMB were significantly elevated compared to normal tissues. GBM patients with higher transcriptional levels of CXCL5/6 were significantly associated with worse disease-free survival, while higher transcriptional levels of CXCL3/5/8 were significantly related to worse overall survival. The functions of CXC chemokines were enriched in Chemokine signaling pathway, Cytokine-cytokine receptor interaction, IL-17 signaling pathway, et.al. RELA and NFKB1were key transcription factors of CXC chemokines. The kinase targets of CXC chemokine contained CDK1, CDK2, PRKCD, MAPK14, ATM, LCK, MTOR, and GRK3, which are involved in oncogenesis, migration, and survival. Moreover, we revealed significant correlations between the expression of CXC chemokines and the infiltration immune cells, especially for dendritic cells.Conclusion The significant CXC chemokines and related pathways may provide a novel possibility for prognostic biomarkers and immunotherapeutic treatment in GMB.Short title: CXC Chemokines with prognosis in GBM

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Dual Functional MicroRNA-186-5p Targets both FGF2 and RelA to Suppress Tumorigenesis of Glioblastoma Multiforme

Cited by 25 publications

References 33 publications

The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA

The Dual Role of miR-186 in Cancers: Oncomir Battling With Tumor Suppressor miRNA

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Identification of Prognostic Biomarkers and Immunotherapeutic Targets with CXC Chemokines in Glioblastoma Multiforme Using Integrated Bioinformatic Analysis

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