Knockdown of miR-210 decreases hypoxic glioma stem cells stemness and radioresistance

Yang, Wei; Wei, Jing; Guo, Tiantian; Shen, Yueming; Liu, Fenju

doi:10.1016/j.yexcr.2014.05.022

Cited by 70 publications

(52 citation statements)

References 47 publications

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“…HIF-2α mRNA and miR-210 expression was increased in hypoxic glioma stem cells (GSCs). Knocking-down of miR-210 inhibited the stemness while induce differentiation and apoptosis in GSCs [37]. One study in MELAS syndrome, a rare neurodegenerative disease caused by mutations in mitochondrial DNA, found that oxidative stress induced expression of miR-9/9*, subsequently decreased the mitochondrial tRNA modification enzymes.…”

Section: Discussionmentioning

confidence: 99%

MiR-9-3p augments apoptosis induced by H2O2 through down regulation of Herpud1 in glioma

Yang

Cui

et al. 2017

PLoS ONE

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MicroRNAs are short, single-stranded non-coding RNA molecules that function as regulators of tumor progression in various cancers, including glioma. The present study sought to investigate the biological functions of miR-9-3p in glioma progression. The results of a microRNA microarray indicated that microRNA-9-3p (miR-9-3p, miR-9*) is down-regulated in high-grade (grades III and IV) gliomas compared with non-tumor tissues. These results were confirmed with real-time PCR. The miR-9-3p expression level was associated with age and tumor grade. Herpud1 was regulated by miR-9-3p in glioma cells and tissues and was identified as a miR-9-3p target with luciferase reporter assays. Glioma cells transfected with miR-9-3p mimics or HERPUD1-RNAi had more apoptotic cells than them in control after induced by H2O2. Our results indicated that low expression of miR-9-3p results in a high level of Herpud1, which may protect against apoptosis in glioma.

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Section: Discussionmentioning

confidence: 99%

MiR-9-3p augments apoptosis induced by H2O2 through down regulation of Herpud1 in glioma

Yang

Cui

et al. 2017

PLoS ONE

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“…In the context of GBM, for instance, miR-210 has been reported to assist cell survival in glioma cell lines (Agrawal et al, 2014; Yang et al, 2014). As a pivotal niche for GICs, hypoxia maintains the distinct biological properties of this specific group of cells.…”

Section: Disscussionmentioning

confidence: 99%

MiR-215 Is Induced Post-transcriptionally via HIF-Drosha Complex and Mediates Glioma-Initiating Cell Adaptation to Hypoxia by Targeting KDM1B

Sun

Wang

et al. 2016

Cancer Cell

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SUMMARY The hypoxic tumor microenvironment serves as a niche for maintaining the glioma-initiating cells (GICs) that are critical for glioblastoma (GBM) occurrence and recurrence. Here we report that hypoxia-induced miR-215 is vital for reprograming GICs to fit the hypoxic microenvironment via suppressing the expression of an epigenetic regulator KDM1B and modulating activities of multiple pathways. Interestingly, biogenesis of miR-215 and several miRNAs is accelerated post-transcriptionally by hypoxia-inducible factors (HIFs) through HIF-Drosha interaction. Moreover, miR-215 expression correlates inversely with KDM1B while positively with HIF1α and GBM progression in patients. These findings reveal a direct role of HIF in regulating miRNA biogenesis and consequently activating the miR-215-KDM1B-mediated signaling required for GIC adaptation to hypoxia.

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“…Consequently, inhibition of miR-210 in hypoxic tumors could restore abnormal tumor blood vessels, improve tumor oxygenation and thus sensitize tumors to radiotherapy. This radiosensitizing effect of miR-210 inhibition has indeed been observed in different tumor types in vitro and in vivo, and CD31 staining of tissues treated with combined miR-210 inhibition and radiotherapy revealed less blood vessels compared to their controls [131, 132, 134, 135]. In general, miR-210 expression promotes angiogenesis in response to hypoxia, indicating a promising therapeutic potential for miR-210 inhibition in combination with radiotherapy.…”

Section: Combination Of Mirna Therapy and Radiotherapymentioning

confidence: 65%

miRNAs: micro-managers of anticancer combination therapies

et al. 2017

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Angiogenesis is one of the hallmarks of cancer progression and as such has been considered a target of therapeutic interest. However, single targeted agents have not fully lived up to the initial promise of anti-angiogenic therapy. Therefore, it has been suggested that combining therapies and agents will be the way forward in the oncology field. In recent years, microRNAs (miRNAs) have received considerable attention as drivers of tumor development and progression, either acting as tumor suppressors or as oncogenes (so-called oncomiRs), as well as in the process of tumor angiogenesis (angiomiRs). Not only from a functional, but also from a therapeutic view, miRNAs are attractive tools. Thus far, several mimics and antagonists of miRNAs have entered clinical development. Here, we review the provenance and promise of miRNAs as targets as well as therapeutics to contribute to anti-angiogenesis-based (combination) treatment of cancer.

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Knockdown of miR-210 decreases hypoxic glioma stem cells stemness and radioresistance

Cited by 70 publications

References 47 publications

MiR-9-3p augments apoptosis induced by H2O2 through down regulation of Herpud1 in glioma

MiR-9-3p augments apoptosis induced by H2O2 through down regulation of Herpud1 in glioma

MiR-215 Is Induced Post-transcriptionally via HIF-Drosha Complex and Mediates Glioma-Initiating Cell Adaptation to Hypoxia by Targeting KDM1B

miRNAs: micro-managers of anticancer combination therapies

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