MiR-181b suppresses proliferation of and reduces chemoresistance to temozolomide in U87 glioma stem cells

Li, Ping; Lu, Xiaoming; Wang, Yingyi; Sun, Lihua; Qian, Chunfa; Yan, Wei; Liu, Ning; You, Yongping; Fu, Zhang

doi:10.1016/s1674-8301(10)60058-9

Cited by 37 publications

(26 citation statements)

References 23 publications

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“…GBM is characterized by complex tissue heterogeneity, in which there is a class of stem cell-like tumor-initiating cells, called GSCs, which have the ability to self-renew, grow continuously and differentiate into multiple neural cell types [34][35][36]. Further studies found that GSCs are key factors leading to the occurrence, recurrence, treatment tolerance and poor prognosis of glioma [35,[37][38][39][40]. We successfully propagated eight human GSC lines with four different molecular subtypes and found the highest PSAP expression and secretion in mesenchymal GSCs, as determined by western blotting and ELISA.…”

Section: Discussionmentioning

confidence: 99%

Prosaposin is a biomarker of mesenchymal glioblastoma and regulates mesenchymal transition through the TGF‐β1/Smad signaling pathway

Jiang

Zhou

Hou

et al. 2019

The Journal of Pathology

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Mesenchymal glioblastoma (GBM) is the most aggressive subtype of GBM. Our previous study found that neurotrophic factor prosaposin (PSAP) is highly expressed and secreted in glioma and can promote the growth of glioma. The role of PSAP in mesenchymal GBM is still unclear. In this study, bioinformatic analysis, western blotting and RT‐qPCR were used to detect the expression of PSAP in different GBM subtypes. Human glioma cell lines and patient‐derived glioma stem cells were studied in vitro and in vivo, revealing that mesenchymal GBM expressed and secreted the highest level of PSAP among four subtypes of GBM, and PSAP could promote GBM invasion and epithelial–mesenchymal transition (EMT)‐like processes in vivo and in vitro. Bioinformatic analysis and western blotting showed that PSAP mainly played a regulatory role in GBM invasion and EMT‐like processes via the TGF‐β1/Smad signaling pathway. In conclusion, the overexpression and secretion of PSAP may be an important factor causing the high invasiveness of mesenchymal GBM. PSAP is therefore a potential target for the treatment of mesenchymal GBM. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd

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Section: Discussionmentioning

confidence: 99%

Prosaposin is a biomarker of mesenchymal glioblastoma and regulates mesenchymal transition through the TGF‐β1/Smad signaling pathway

Jiang

Zhou

Hou

et al. 2019

The Journal of Pathology

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“…With this knowledge, microRNAs reported to influence TMZ resistance in GBM (miR-195, miR-455, miR-10 (Ujifuku et al 2010), miR-181b (Li et al 2010; Slaby et al 2010), miR-21 (Shi et al 2010a; Wong et al 2012), miR-125b (Shi et al 2012), miR-145 (Yang et al 2012), miR-211 (Asuthkar et al 2012), miR-17 (Comincini et al 2013), miR-9 (Munoz et al 2013), the miR-183/96/182 cluster (Tang et al 2013), and miR-221/222 (Chen et al 2012c)) were shown to target pathways involved in proliferation, apoptosis, and stem cell maintenance. Some studies suggested that targeting GSCs may effectively reduce tumor recurrence and significantly improve GBM sensitization to radiation (Huang et al 2010).…”

Section: Micrornas In Brain Tumorsmentioning

confidence: 99%

Extracellular Vesicles and MicroRNAs: Their Role in Tumorigenicity and Therapy for Brain Tumors

2016

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MicroRNAs are small non-coding RNAs which mediate post-transcriptional gene regulation. Recently, microRNAs have also been found to be localized to the extracellular space, often encapsulated in secreted extracellular vesicles (EVs). This tandem of EVs and tissue-specific expressed/secreted microRNAs that can be taken up by neighboring or distant recipient cells, leading to changes in gene expression—suggests a cell-specialized role in physiological and pathological conditions. The complexity of solid tumors and their distinct pathophysiology relies on interactive communications between the various cell types in the neoplasm (tumor, endothelial, or macrophages, for instance). Understanding how such EV/microRNA-mediated communication occurs may actually lead to avenues for therapeutic exploitation and/or intervention, particularly for the most formidable cancers, such as those in the brain. In this review, the role of microRNAs/EVs in brain tumors will be discussed with emphasis on how these molecules could be utilized for tumor therapy.

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“…Many miRNAs have been proved to be proto-oncogenes or tumor suppressors in various human cancers, including in glioma. [3][4][5] Recent studies have revealed that miRNAs, such as miR-7, 6, 7 miR-124, [8][9][10] miR-128, 11 miR-107, 12 and miR-181b, [13][14][15] are globally dysregulated in glioma. However, the particular molecular mechanisms through which miRNAs mediate glioma carcinogenesis and metastasis are still largely unknown.…”

Section: Introductionmentioning

confidence: 99%

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

Wang

Wei

Tong

et al. 2015

Cancer Biology & Therapy

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Glioma is the most common malignant brain tumors with poor prognosis. The molecular events involved in the development and progression of glioma remain unclear. In this study, the expression levels of miR-302c-3p were examined in glioma tissues by qRT-PCR. The in vitro and in vivo functional effects of miR-302c-3p were examined further. Luciferase reporter assays were conducted to confirm the targeting associations. Results showed that the expression level of miR-302c-3p in glioma tissues was significantly lower than those in normal brain tissues (P < 0.001). The decreased expression of mi-302c-3p in glioma was positively associated with WHO grade (P < 0.001). Up-regulation of MTDH was also detected in glioma tumors compared with normal brain tissues (P = 0.0027) and is inversely correlated with miR-302c-3p expression (P = 0.003, R(2) = 0.4065). MTDH mRNA is a direct target of miR-302c-3p, whose ectopic expression decreases MTDH expression through binding to its 3'-untranslated region. Overexpression of miR-302c-3p results in a dramatic inhibition of glioma cells proliferation and invasion in vitro and in vivo. These data suggest that miR-302c-3p play a pivotal role in the progression of glioma by targeting MTDH and is a potential inhibitor in glioma treatment.

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MiR-181b suppresses proliferation of and reduces chemoresistance to temozolomide in U87 glioma stem cells

Cited by 37 publications

References 23 publications

Prosaposin is a biomarker of mesenchymal glioblastoma and regulates mesenchymal transition through the TGF‐β1/Smad signaling pathway

Prosaposin is a biomarker of mesenchymal glioblastoma and regulates mesenchymal transition through the TGF‐β1/Smad signaling pathway

Extracellular Vesicles and MicroRNAs: Their Role in Tumorigenicity and Therapy for Brain Tumors

MiR-302c-3p suppresses invasion and proliferation of glioma cells via down-regulating metadherin (MTDH) expression

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