miRNA-182 and the regulation of the glioblastoma phenotype - toward miRNA-based precision therapeutics

Kouri, Fotini M.; Ritner, Carissa; Stegh, Alexander H.

doi:10.1080/15384101.2015.1093711

Cited by 45 publications

(34 citation statements)

References 62 publications

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“…In recent years, various delivery mechanisms have been investigated, for example, miRNAs can be conjugated to modified gold nanoparticles, which are able to carry miRNAs across the blood-brain barrier, as in the case of miR-182 [ 29 ]. Gold nanoparticles also demonstrate low toxicity, high stability and high cell uptake, making them the most promising delivery tool for miRNAs [ 92 ]. Other delivery mechanisms available include, adeno-associated virus [ 93 ], polymeric brain-penetrating nano-particles [ 94 ] and mesenchymal stem cells [ 95 , 96 ].…”

Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma

Cruickshanks

Zhang

Yuan

et al. 2017

Cancers

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Glioblastoma (GBM) is a lethal brain tumor with dismal prognosis. Current therapeutic options, consisting of surgery, chemotherapy and radiation, have only served to marginally increase patient survival. Receptor tyrosine kinases (RTKs) are dysregulated in approximately 90% of GBM; attributed to this, research has focused on inhibiting RTKs as a novel and effective therapy for GBM. Overexpression of RTK mesenchymal epithelial transition (MET), and its ligand, hepatocyte growth factor (HGF), in GBM highlights a promising new therapeutic target. This review will discuss the role of MET in cell cycle regulation, cell proliferation, evasion of apoptosis, cell migration and invasion, angiogenesis and therapeutic resistance in GBM. It will also discuss the modes of deregulation of HGF/MET and their regulation by microRNAs. As the HGF/MET pathway is a vital regulator of multiple pro-survival pathways, efforts and strategies for its exploitation for GBM therapy are also described.

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Section: Conclusion and Future Perspectivesmentioning

confidence: 99%

Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma

Cruickshanks

Zhang

Yuan

et al. 2017

Cancers

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“…It can regulate the expressions of different target genes, and a series of physiological processes such as growth, development, and cell differentiation. It plays the role of oncogene or tumor suppressor gene in the process of malignant tumor [12][13][14]. Studies have confirmed that miR-182 is abnormally expressed in a variety of solid malignancies, including lung cancer, pancreatic cancer, cholangiocarcinoma, colorectal cancer, prostate cancer, liver cancer, and breast cancer.…”

Section: Introductionmentioning

confidence: 99%

MiR-182 regulates cell proliferation and apoptosis in laryngeal squamous cell carcinoma by targeting the CRR9

et al. 2019

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Correspondence: Hongxia Deng (msrqvbo5805551@126.com) Background: The effect of miR-182 on the expressions of CRR9 in laryngeal squamous cell carcinoma (LSCC) cells, and the impact on invasion and metastasis of LSCC were investigated in the present paper. Methods: The expressions of miR-182 in LSCC tissue and cell line were detected by RT-qPCR. MTT assay and Annexin V staining were used to detect the effects of miR-182 on tumor cells proliferation. Target gene prediction and screening, and luciferase reporter assay were designed to verify downstream target genes of miR-182. The mRNA and protein expressions of CRR9 were detected by qRT-PCR and Western blot. Finally, the expressions of CRR9 were measured by transfecting cells with miR-182 in mice. Results: Compared with normal tissue and cell, the expressions of miR-182 in tumor tissues and cells were much lower. Over-expressions of miR-182 can increase apoptosis rate. Luciferase reporter assay revealed that CRR9 was a downstream gene of miR-182. Reintroduction of CRR9 abolished miR-182-induced LSCC cell growth inhibition. In animal models, over-expressions of miR-182 can reduce tumor weight and promote apoptosis. Conclusion: miR-182 can inhibit the proliferation of LSCC cells by directly inhibiting the expressions of CRR9, thereby suppressing the occurrences and developments of LSCC.

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“…Most miRNAs in c-Met signaling are antioncogenic. Besides above, there are antioncogenic miRNAs include miR-410, -598, -182, and -144-3p in nervous system (Chen et al, 2012;Kouri et al, 2015;Lan et al, 2015;; miR-140-5p in retinoblastoma (Liao et al, 2018) and miR-144 in uveal melanoma (Sun et al, 2015c); miR-365-3p, -152, -23b, -27b, and -143 in oral squamous cell carcinoma (OSCC) Fukumoto et al, 2016;Li et al, 2018a;Huang et al, 2019). MiR-449b and -3666 are downregulated in thyroid cancer (Chen et al, 2015a;Wang et al, 2016); and miR-133b, -340, -335, and -185 are inhibit tumor progression in breast cancer (Wu et al, 2011;Fu et al, 2014;Gao et al, 2015;Wang Q. Y. et al, 2018).…”

Section: Other Antioncogenic Mirnas and C-metmentioning

confidence: 99%

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

Zhan

Zhang

et al. 2020

Front. Cell Dev. Biol.

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MicroRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are components of many signaling pathways associated with tumor aggressiveness and cancer metastasis. Some lncRNAs are classified as competitive endogenous RNAs (ceRNAs) that bind to specific miRNAs to prevent interaction with target mRNAs. Studies have shown that the hepatocyte growth factor/mesenchymal-epithelial transition factor (HGF/c-Met) pathway is involved in physiological and pathological processes such as cell growth, angiogenesis, and embryogenesis. Overexpression of c-Met can lead to sustained activation of downstream signals, resulting in carcinogenesis, metastasis, and resistance to targeted therapies. In this review, we evaluated the effects of anti-oncogenic and oncogenic non-coding RNAs (ncRNAs) on c-Met, and the interactions among lncRNAs, miRNAs, and c-Met in cancer using clinical and tissue chromatin immunoprecipition (ChIP) analysis data. We summarized current knowledge of the mechanisms and effects of the lncRNAs/miR-34a/c-Met axis in various tumor types, and evaluated the potential therapeutic value of lncRNAs and/or miRNAs targeted to c-Met on drug-resistance. Furthermore, we discussed the functions of lncRNAs and miRNAs in c-Met-related carcinogenesis and potential therapeutic strategies.

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miRNA-182 and the regulation of the glioblastoma phenotype - toward miRNA-based precision therapeutics

Cited by 45 publications

References 62 publications

Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma

Role and Therapeutic Targeting of the HGF/MET Pathway in Glioblastoma

MiR-182 regulates cell proliferation and apoptosis in laryngeal squamous cell carcinoma by targeting the CRR9

MicroRNAs and Long Non-coding RNAs in c-Met-Regulated Cancers

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