miR‑124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

Meng, Yun; Shang, Fei; Zhu, Ye

doi:10.3892/etm.2019.7914

Cited by 6 publications

(3 citation statements)

References 23 publications

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“…As expected, knockdown of Nogo-A and inhibition of the Nogo-A/NgR signaling pathway decreased malignant behavior, including cell proliferation, invasion and tumor formation in soft agar. Nogo-A/NgR signaling pathway was associated with the inhibition of the proliferation and differentiation in glioblastoma stem cells ( 27 ); however, in this study, following Nogo-A knockdown and Nogo-A/NgR pathway inhibition, the stemness of CSCs derived from U87MG glioblastoma cells were inhibited, which is in disagreement with the previous report ( 27 ). This could be due to the use of different CSCs enrichment methods, which could result in different sub-populations of CSCs.…”

Section: Discussioncontrasting

confidence: 99%

Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells

Zhou

et al. 2022

Oncol Lett

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Neurite outgrowth inhibitor A (Nogo-A), a member of the reticulon 4 family, is an axon regeneration inhibitor that is negatively associated with the malignancy of oligodendroglial tumors. It has been suggested that the Nogo-A/Nogo Receptor (NgR) pathway plays a promoting effect in regulating cancer stem-like cells (CSCs) derived from glioblastoma, indicating that Nogo-A could exert different roles in CSCs than those in parental cancer cells. In the present study, CSCs were generated from the human Uppsala 87 malignant glioma (U87MG) cell line. These U87MG-CSCs were characterized by the upregulation of CD44 and CD133, which are two markers of stemness. The expression levels of Nogo-A and the differentiation of U87MG-CSCs were investigated. In addition, the proliferation, invasion and colony formation U87MG-CSCs were examined. Using culture in serum-containing medium, U87MG-CSCs were differentiated into neuron-like cells specifically expressing MAP2, β-III-tubulin and nestin. Nogo-A was upregulated in U87MG-CSCs compared with parental cells. Knockdown of Nogo-A and inhibition of the Nogo-A/NgR signaling pathway in U87MG-CSCs markedly decreased cell viability, cell cycle entry, invasion and tumor formation, indicating that Nogo-A could regulate U87MG-CSC function. Moreover, Nogo-A was involved in intracellular ATP synthesis and scavenging of accumulated reactive oxygen species. Nogo-A/NgR pathway exerted protective effects against hypoxia-induced non-apoptotic and apoptotic cell death. These results suggest that Nogo-A plays an important role in regulating U87MG-CSCs via the Nogo-A/NgR signaling pathway. Nogo-A may also different roles in U87MG-CSCs compared with their parental cells.

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Section: Discussioncontrasting

confidence: 99%

Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells

Zhou

et al. 2022

Oncol Lett

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“…Glioma derived from glial cells is the most common malignant tumor of the central nervous system and accounts for more than half of all malignant brain tumors [ 1 , 2 ]. The clinical features of malignant glioma include poor prognosis, high recurrence rate, and high mortality [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Prognostic role of METTL1 in glioma

Yang

Wang

et al. 2021

Cancer Cell Int

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Background Current treatment options for glioma are limited, and the prognosis of patients with glioma is poor as the available drugs show low therapeutic efficacy. Furthermore, the molecular mechanisms associated with glioma remain poorly understood. METTL1 mainly catalyzes the formation of N(7)-methylguanine at position 46 of the transfer RNA sequence, thereby regulating the translation process. However, the role of METTL1 in glioma has not been studied to date. The purpose of this study was to analyze the expression and prognosis of METTL1 in glioma, and to explore the potential analysis mechanism. Methods Data from five publicly available databases were used to analyze METTL1 expression across different tumor types and its differential expression between carcinoma and adjacent normal tissues. The expression of METTL1 in glioma was further validated using real-time polymerase chain reaction and immunohistochemistry. Meanwhile, siRNA was used to knockdown METTL1 in U87 glioma cells, and the resultant effect on glioma proliferation was verified using the Cell Counting Kit 8 (CCK8) assay. Furthermore, a nomogram was constructed to predict the association between METTL1 expression and the survival rate of patients with glioma. Results METTL1 expression increased with increasing glioma grades and was significantly higher in glioma than in adjacent noncancerous tissues. In addition, high expression of METTL1 promoted cell proliferation. Moreover, METTL1 expression was associated with common clinical risk factors and was significantly associated with the prognosis and survival of patients with glioma. Univariate and multivariate Cox regression analyses revealed that METTL1 expression may be used as an independent prognostic risk factor for glioma. Furthermore, results of functional enrichment and pathway analyses indicate that the mechanism of METTL1 in glioma is potentially related to the MAPK signaling pathway. Conclusions High METTL1 expression is significantly associated with poor prognosis of patients with glioma and may represent a valuable independent risk factor. In addition, high expression of METTL1 promotes glioma proliferation and may regulate mitogen-activated protein kinase (MAPK) signaling pathway. Thus, METTL1 may be a potential biomarker for glioma. Further investigations are warranted to explore its clinical use.

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“…MicroRNAs are single strand small noncoding RNAs that partially or completely bind to the 3′-UTR region of target mRNAs to modulate gene expression, resulting in the regulation of proliferation, differentiation, apoptosis and metastasis in cancer cell progression [10,11]. MiR-124 expression has been reported to be widely downregulated in many cancers, such as breast cancer, colon cancer, glioma, lymphoma, NSCLC and so on [12][13][14][15][16]. Accumulating reports have demonstrated the roles of miR-124 in the occurrence and development of a variety of tumors.…”

Section: Introductionmentioning

confidence: 99%

AKT2 drives cancer progression and is negatively modulated by miR-124 in human lung adenocarcinoma

Liu

Zhu

et al. 2020

Respir Res

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Background: AKT2 is highly expressed in many human cancers, including non-small cell lung cancer (NSCLC). Accumulating evidence has also revealed that AKT2 can promote NSCLC cell proliferation and metastasis. However, the involved mechanism remains unclear. Herein, our study mainly explored the function of AKT2 during cancer progression and uncovered a new post-transcriptional mechanism of AKT2 expression in lung adenocarcinoma (LUAD). Methods: Quantitative real-time (qRT-PCR), western blot and immunohistochemistry (IHC) assays were performed to detect the expression of AKT2 and other proteins. Cell counting kit-8 (CCK-8), colony formation and EdU assays were performed to assess cell proliferation. Flow cytometry analysis was used to detect changes in the cell cycle and apoptosis. Transwell assays were used to evaluate cell migration and invasion. Additionally, a luciferase reporter assay and western blotting were employed to assess miR-124 targeting of AKT2. Xenograft mouse model was used to observe the role of miR-124/AKT2 axis on the occurrence and development of LUAD. Results: We showed that AKT2 was highly expressed in NSCLC tissues and closely related to the poor prognosis of LUAD patients. Moreover, AKT2 affected LUAD cell proliferation, migration and invasion by regulating the cell cycle and promoting the occurrence of epithelial-mesenchymal transition (EMT) and the expression of matrix metalloproteinases (MMPs). In addition, we demonstrated that miR-124 overexpression downregulated AKT2 expression by binding to the 3′-untranslated region (3′-UTR) of AKT2 and thus inhibited the occurrence and development of LUAD in vivo and in vitro. Conclusions: Our results suggest that miR-124 overexpression can negatively regulate AKT2 and thus inhibit the progression of LUAD. Therefore, the miR-124/AKT2 axis may serve as a potential target for novel therapies for LUAD.

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miR‑124 participates in the proliferation and differentiation of brain glioma stem cells through regulating Nogo/NgR expression

Cited by 6 publications

References 23 publications

Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells

Nogo‑A/NgR signaling regulates stemness in cancer stem‑like cells derived from U87MG glioblastoma cells

Prognostic role of METTL1 in glioma

AKT2 drives cancer progression and is negatively modulated by miR-124 in human lung adenocarcinoma

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