The significance of microRNA-184 on JAK2/STAT3 signaling pathway in the formation mechanism of glioblastoma

Zhang, Xuekui; Ding, Huaiyu; Yao, Han; Sun, De‑Ke; Wang, Haitao; Zhai, Xiaoxiang

doi:10.3892/ol.2015.3798

Cited by 8 publications

(7 citation statements)

References 13 publications

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“…Moreover, miRNAs are abnormally expressed in various cancers and closely related with cancer initiation and progression (14)(15)(16). They also act as tumour suppressors or promoters by directly targeting known oncogenes or tumour suppressor genes (17)(18)(19). Therefore, identifying specific miRNAs that play important roles in tumourigenesis and tumour development might provide therapeutic biomarkers for cancer diagnosis, prognosis and therapy.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-342 inhibits the progression of glioma by directly targeting PAK4

Wang

et al. 2017

Oncology Reports

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Glioma is an extremely aggressive and lethal type of brain tumour that originates from glial cells. MicroRNA (miRNA) dysregulation has been implicated in the occurrence and progression of many human cancers, including glioma. Thus, some specific miRNAs are potential therapeutic targets for glioma diagnosis, therapy and prognosis. MicroRNA-342 (miR‑342) has been reported to be abnormally expressed in various types of cancer. However, the precise roles of miR‑342 in glioma remain unknown. The present study showed that miR‑342 is relatively downregulated in glioma tissues and cell lines compared with that in adjacent normal tissues and normal human astrocytes. We observed that low miR‑342 expression levels are correlated with advanced WHO grades and low KPS scores of glioma patients. In addition, the results of the functional assays demonstrated that miR‑342 overexpression inhibits the proliferation and invasion of glioma cells and induces apoptosis. Further investigation revealed that P21 activated kinases 4 (PAK4) is a direct target of miR‑342 in glioma. PAK4 was significantly upregulated in glioma tissues and inversely correlated with miR‑342 expression. Moreover, PAK4 knockdown can mimic the effects of miR‑342 on glioma cell proliferation, invasion and apoptosis. Notably, restoration of expression of PAK4 reversed the suppressive effects induced by the miR‑342 in the glioma cells. The upregulation of miR‑342 inactivated the AKT and ERK pathways in glioma. These findings may contribute to the understanding of the molecular mechanism underlying the carcinogenesis and progression of glioma, and to provide novel therapeutic target for the treatment of glioma patients.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-342 inhibits the progression of glioma by directly targeting PAK4

Wang

et al. 2017

Oncology Reports

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“…In particular, JAK2/STAT3 pathway is deeply involved in the survival and motion of tumor cells [35]. The excessive activation of JAK2 signaling in glioma is accelerated by abnormal signals from upstream regulators [36,37]. This usually involves any gain-of-function mutations or up-regulation of upstream inhibitors, and, on the other hand, any loss-of function mutation or down-regulation of the upstream inhibitors.…”

Section: Discussionmentioning

confidence: 99%

CTR9-Mediated JAK2/STAT3 Pathway Promotes The Proliferation, Migration and Invasion of Human Glioma Cells

Chen

et al. 2021

Preprint

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Background CTR9 (Cln three requiring 9) has been reported to be implicated in protein modification and oncogenesis of several human cancers. However, the protein expression and mechanism of CTR9 in glioma progression remain unclear. Methods We analyzed mRNA expression of CTR9 and CTR9-related survival curves in the public database. Then we detected CTR9 expression in glioma tissues and constructed U251 and U87 cells with stable silencing or overexpression of CTR9. Cell function tests and Western blot were conducted to explore the effects of CTR9 on glioma proliferation, invasion and migration, as well as the specific mechanism. All the date was presented as means ± SEM. Two-sample t-test and one-way analysis of variance (ANOVA) were used to identify whether there was a significant difference between each group of data. Results We found that CTR9 was overexpressed in glioma and inversely associated with glioma patient survival. The results manifested that knockdown of CTR9 suppressed the proliferation, migration and invasion of glioma cells, while overexpression facilitated them. The underlying molecular mechanism may involve the regulation of JAK2/STAT3 pathway by CTR9. Conclusion Our present study indicates that CTR9 is highly expressed in glioma and related to glioma grading and prognosis. CTR9 regulates malignant behaviors of glioma cells by activating JAK2/STAT3 pathway. Therefore, CTR9 is a promising biomarker for the diagnosis,targeted therapy and prognosis evaluation of glioma.

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“…The present study reported that in vitro proliferation and invasive ability of osteosarcoma U-2OS cells and 143B cells transfected with miR-184 analogue sequence were markedly enhanced, which was consistent with a previous study regarding the regulatory effect of miR-184 on osteosarcoma cell lines ( 21 ). MiR-184 has been demonstrated to promote the proliferation and invasion of glioblastoma ( 38 ). Su et al ( 16 ) reported that miR-184 may function as a tumor suppressor in renal cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Regulatory effects of microRNA‑184 on osteosarcoma via the Wnt/β‑catenin signaling pathway

Wang

et al. 2018

Mol Med Report

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The present study aimed to investigate the role of microRNA (miRNA/miR)-184 in osteosarcoma growth, development and metastasis, and the effects of miRNA-184 on the proliferation, invasion and metastasis of osteosarcoma cells and associated mechanisms. In vitro, miR-184 was transfected into U-2OS cells and 143B cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of miR-184. MTT was utilized to detect cell proliferation. A Transwell assay was applied to detect cell invasiveness. In vivo, an osteosarcoma tibial orthotopic metastatic tumor model was established, and western blotting and RT-qPCR were used to detect the expression of Wnt and β-catenin. Following the overexpression of miR-184, the proliferation and cell invasion ability were significantly increased in U-2OS and 143B cells. Following inhibition of miR-184, cell proliferation and cell invasion ability were significantly decreased. In nude mice, tumor volume significantly increased following overexpression of miR-184, and Wnt and phosphorylated β-catenin levels were significantly increased. Following miR-184 inhibition, tumor volume was significantly decreased, and Wnt and phosphorylated β-catenin levels were significantly decreased. The results of the present study indicated that the Wnt/β-catenin signaling pathway serves a key function in the mechanism of osteosarcoma. Inhibition of miRNA-184 may reduce tumor volume of osteosarcoma via regulation of the Wnt/β-catenin signaling pathway and may provide a novel strategy for the future diagnosis and treatment of osteosarcoma.

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The significance of microRNA-184 on JAK2/STAT3 signaling pathway in the formation mechanism of glioblastoma

Cited by 8 publications

References 13 publications

MicroRNA-342 inhibits the progression of glioma by directly targeting PAK4

MicroRNA-342 inhibits the progression of glioma by directly targeting PAK4

CTR9-Mediated JAK2/STAT3 Pathway Promotes The Proliferation, Migration and Invasion of Human Glioma Cells

Regulatory effects of microRNA‑184 on osteosarcoma via the Wnt/β‑catenin signaling pathway

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