Genome Editing Reveals Glioblastoma Addiction to MicroRNA-10b

Fatimy, Rachid El; Subramanian, Shruthi; Uhlmann, Erik J.; Krichevsky, Anna M.

doi:10.1016/j.ymthe.2016.11.004

Cited by 84 publications

(74 citation statements)

References 37 publications

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“…Besides, the expression of microRNA-10b in patients with metastasis, including lymph node metastasis, was significantly higher than that in patients without metastasis. The up-regulation of microRNA-10b has been shown to promote the invasion and metastasis of various tumors [23][24][25][26][27][28][29]. In this study, the knockdown of miR-10b expression inhibited the growth, migration and invasion of HGC27 cells.…”

Section: Discussionmentioning

confidence: 71%

“…microRNA-10b is located in the HOX gene cluster on chromosome 2, which is closely related to tumor invasion and metastasis. Previous studies have shown that microRNA-10b is overexpressed in breast cancer [23], colorectal cancer [24], head and neck cancer [25], pancreatic cancer [26], glioblastoma [27], nasopharyngeal carcinoma [28], hepatocellular carcinoma [29] and so on. Consistent with previous reports, this study showed that the expression of microRNA-10b in GC tissues and 6 GC cell lines was higher than that in paracancerous non-tumor tissues and GES-1 cell line.…”

Section: Discussionmentioning

confidence: 99%

“…Taken together, these results were consistent with the previous findings, showing that microRNA-10b promoted the metastasis of GC [38][39][40][41], suggesting that microRNA-10b exerted oncogenic activity in GC cells, however, the mechanism by which it drives tumor metastasis is unclear. Previous studies have revealed that microRNA-10b promotes the metastasis of a variety of tumor cells by regulating Bim, TFAP2C, P16, P21, E-cadherin, CD138, RHOC, RhoC, uPAR, MMP-2, MMP-9, HOXD10, etc [23][24][25][26][27][28][29]. In this study, microRNA-10b was involved in the proliferation and metastasis of GC cells by targeting CSMD1, and facilitated epithelial-mesenchyma transformation (EMT) process by the NF-κB pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence has shown that miRNAs can modulate tumor growth, metastasis, and progression by regulating multiple target genes [20][21][22]. microRNA-10b has been found to be highly expressed in many malignant tumours and related to the progress of breast cancer [23], colorectal cancer [24], head and neck cancer [25], pancreatic adenocarcinoma [26], glioblastoma [27], nasopharyngeal cancer [28], and liver cancer [29]. The pleiotropic nature of microRNA-10b was due to its suppression of multiple tumor suppressors, including ras homolog family member C (RhoC), urokinase plasminogen activator receptor (uPAR), matrix metalloproteinases (MMPs), tumor protein p53 (TP53), forkhead box O3 (FOXO3), CYLD lysine 63 deubiquitinase (CYLD), paired box 6 (PAX6), patched 1 (PTCH1), homeobox D10 (HOXD10), notch receptor 1 (NOTCH1), BCL6 transcription repressor (Bcl-6), and Kruppel like factor 4 (KLF4) [29][30][31][32][33].…”

Section: Introductionmentioning

confidence: 99%

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Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

et al. 2019

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Aim:This study aimed to investigate the oncogenic activity of microRNA-10b by targeting CUB and sushi multiple domains protein 1 (CSMD1) in human gastric cancer (GC) and the underlying mechanisms. Methods: The expression of CSMD1 in human GC tissues was evaluated by real-time reverse transcription polymerase chain reaction (RT-PCR), immunoblotting, and immunohistochemical analysis. The expressive abundance of microRNA-10b was detected by stem-loop RT-PCR. Molecular and cellular techniques, including lentiviral vector-mediated knockdown or overexpression, were used to elucidate the effect of microRNA-10b on the expression of CSMD1. Results: CSMD1 was targeted and downregulated by microRNA-10b in human GC tissues and cells, and the down-regulated expression of CSMD1 contributed to poor survival. The knockdown of microRNA-10b expression inhibited cell proliferation in GC cells in vitro and tumor growth in vivo. The inhibition of microRNA-10b expression repressed invasion and migration of HGC27 cells and retarded GC cells metastasis to the liver in Balb/c nude mice. The up-regulated expression of microRNA-10b promoted the proliferation and metastasis of MKN74 cell in vitro. Intratumoral injection of microRNA-10b mimic also promoted the growth and metastasis of tumor xenografts in Balb/c nude mice. Mechanistically, microRNA-10b promoted the invasion and metastasis of human GC cells through inhibiting the expression of CSMD1, leading to the activation of the nuclear factor-κB (NF-κB) pathway that links inflammation to carcinogenesis, subsequently resulting in the upregulation of c-Myc, cyclin D1 (CCND1), and epithelial-mesenchymal transition (EMT) markers. Conclusions: The findings established that microRNA-10b is an oncomiR that drives metastasis. Moreover, a set of critical tumor suppressor mechanisms was defined that microRNA-10b overcame to drive human GC progression.

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Section: Discussionmentioning

confidence: 71%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

et al. 2019

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“…The relevance of these findings is not only that GBM EVs could modify neighboring astrocytes to induce tumor-supportive functions, but, importantly enough, GBM EVs may drive astrocytes to become tumorigenic themselves. GBM EVs' contents include oncogenic proteins and regulators, such as EGFRvIII (mRNA and protein), miR-10b or miR-21 [23,38,68], which could induce the malignant transformation of astrocytes. Indeed, in the above mentioned study by Oushy and colleagues [59], GBM EVs drove significant molecular changes in astrocytes that resemble cancer signaling pathways, and reduced astrocyte dependence on anchorage to a solid matrix, an indicator of cellular transformation.…”

Section: Effects On Astrocytesmentioning

confidence: 99%

Extracellular Vesicle-Mediated Communication between the Glioblastoma and Its Microenvironment

Matarredona

Pastor

2019

Cells

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The glioblastoma is the most malignant form of brain cancer. Glioblastoma cells use multiple ways of communication with the tumor microenvironment in order to tune it for their own benefit. Among these, extracellular vesicles have emerged as a focus of study in the last few years. Extracellular vesicles contain soluble proteins, DNA, mRNA and non-coding RNAs with which they can modulate the phenotypes of recipient cells. In this review we summarize recent findings on the extracellular vesicles-mediated bilateral communication established between glioblastoma cells and their tumor microenvironment, and the impact of this dialogue for tumor progression and recurrence.

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microRNA‐based diagnostic and therapeutic applications in cancer medicine

2021

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It has been almost two decades since the first link between microRNAs and cancer was established. In the ensuing years, this abundant class of short noncoding regulatory RNAs has been studied in virtually all cancer types. This tremendously large body of research has generated innovative technological advances for detection of microRNAs in tissue and bodily fluids, identified the diagnostic, prognostic, and/or predictive value of individual microRNAs or microRNA signatures as potential biomarkers for patient management, shed light on regulatory mechanisms of RNA-RNA interactions that modulate gene expression, uncovered cell-autonomous and cell-to-cell communication roles of specific microRNAs, and developed a battery of viral and nonviral delivery approaches for therapeutic intervention. Despite these intense and prolific research efforts in preclinical and clinical settings, there are a limited number of microRNA-based applications that have been incorporated into clinical practice. We review recent literature and ongoing clinical trials that highlight most promising approaches and standing challenges to translate these findings into viable microRNA-based clinical tools for cancer medicine.

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Genome Editing Reveals Glioblastoma Addiction to MicroRNA-10b

Cited by 84 publications

References 37 publications

Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

Deregulation of CSMD1 targeted by microRNA-10b drives gastric cancer progression through the NF-κB pathway

Extracellular Vesicle-Mediated Communication between the Glioblastoma and Its Microenvironment

microRNA‐based diagnostic and therapeutic applications in cancer medicine

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