MicroRNA-1225-5p behaves as a tumor suppressor in human glioblastoma via targeting of IRS1

Li, Dongyuan; Chi, Guonan; Chen, Zhuo; Jin, Xiaogao

doi:10.2147/ott.s178001

Cited by 21 publications

(15 citation statements)

References 37 publications

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“…As a member of miRNAs, the action of miR-1225-5p in cancer has been widely reported, including its antitumor effect in glioblastoma [21]. Our data confirmed that miR-1225-5p was expressed at low levels and inhibited the cell viability in glioblastoma, which is consistent with the conclusion that miR-1225-5p is a tumor suppressor of glioblastoma.…”

Section: Discussionsupporting

confidence: 89%

“…Overexpression of FNDC3B prevents the miR-1225-5pmediated suppression on malignant phenotype of glioblastoma cells. It has been reported that miR-1225-5p can inhibit cell viability and functioned as a tumor suppressor in glioblastoma [21], which was also verified by the aforementioned biological experiments. So as to explore whether this repressive function was realized by regulating FNDC3B, CCK-8 and transwell experiments were performed.…”

Section: Resultssupporting

confidence: 63%

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MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

Wang

Zhang

et al. 2020

Open Medicine

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This study attempted to research the molecular mechanism underlying the inhibitory role of miR-1225-5p in the malignant progression of glioblastoma. Bioinformatics analyses based on the gene expression omnibus (GEO) and Chinese glioma genome atlas (CGGA) databases showed that miR-1225-5p, as a favorable prognostic factor, was expressed at low levels in glioblastoma, and its expression was also related to WHO grade and age. The subsequent CCK-8 assay indicated that miR-1225-5p might prevent the malignant progression of glioblastoma, which was represented by that miR-1225-5p mimic reduced the viability of glioblastoma cells. Then, we predicted that FNDC3B might be a potential target gene of miR-1225-5p, and it was negatively correlated with the level of miR-1225-5p, which were confirmed by dual-luciferase reporter assay, qRT-PCR and western blot assays. Moreover, based on the analyses of the cancer genome atlas (TCGA), Oncomine and CGGA databases, FNDC3B was enriched in glioblastoma and high expression of FNDC3B led to poor prognosis. Finally, CCK8 and transwell experiments showed that the ability of miR-1225-5p to inhibit glioblastoma cell viability, invasion and migration was at least partially achieved by targeting FNDC3B. In general, these results revealed that the miR-1225-5p/FNDC3B axis contributes to inhibiting the malignant phenotype of glioblastoma cells, which lays a foundation for molecular diagnosis and treatment of glioblastoma.

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Section: Discussionsupporting

confidence: 89%

Section: Resultssupporting

confidence: 63%

MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

Wang

Zhang

et al. 2020

Open Medicine

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“…25 Expression of several miRNAs has been reported to be dysregulated in GBM and to play a significant part in GBM formation and progression. [26][27][28] MiRNAs may perform tumorsuppressive or tumor-promoting functions in GBM through regulation of the expression of their target genes. 29 Hence, elucidation of the functions of cancerassociated miRNAs in GBM may facilitate the identification of promising therapeutic targets in GBM.…”

Section: Discussionmentioning

confidence: 99%

<p>MicroRNA-559 plays an inhibitory role in the malignant progression of glioblastoma cells by directly targeting metadherin</p>

Yang¹,

Zhang²,

Xu³

et al. 2019

OTT

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Purpose: Several microRNAs (miRNAs) that are aberrantly expressed in glioblastoma multiforme (GBM) play a significant role in GBM formation and progression. The expression profile and functions of miR-559 in GBM remain unclear. Here, we quantified the expression and investigated the involvement of miR-559 in the oncogenicity of GBM cells in vitro and in vivo. Material and methods: Reverse-transcription quantitative polymerase chain reaction (RT-qPCR) was carried out to determine miR-559 expression in GBM tissues and cell lines. A series of functional assays was performed to evaluate the effects of miR-559 overexpression on GBM cell proliferation, apoptosis, migration, and invasion in vitro and on GBM tumor growth in vivo. The regulatory mechanisms of miR-559 action in GBM cells were then explored. Results: The expression of miR‑559 was lower in GBM tissues and cell lines and significantly correlated with the Karnofsky performance score and tumor size among patients with GBM. Exogenous miR‑559 expression inhibited GBM cell proliferation, migration, and invasion and promoted apoptosis. MiR-559 overexpression decreased tumor growth in vivo. Mechanistic experiments confirmed metadherin ( MTDH ) as a direct target gene of miR-559 in GBM. Silencing of MTDH induced effects similar to those of miR-559 upregulation in GBM cells, whereas MTDH expression restoration attenuated the antitumor effects of miR‑559 in GBM cells. Protein kinase B (AKT) in the phosphatase and tensin homolog (PTEN)–AKT signaling pathway was found to be deactivated in GBM cells after upregulation of miR-559 both in vitro and in vivo. Conclusion: MiR-559 acts as a tumor suppressor in GBM cells in vitro and in vivo, at least in part through the downregulation of MTDH and inhibition of AKT in the PTEN–AKT pathway. Therefore, targeting the miR-559–MTDH axis may be a promising therapeutic strategy for patients with GBM.

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“…Increased expression levels of IGF-1R and IRS1 are associated with many human malignancies which implies that both of the proteins have a pivotal role in carcinogenesis (9,21,22). Recent studies have also shown that IGF-1R and IRS1 are responsible for the development of chemo-and radioresistance in cancer cells but their molecular mechanisms have not been discovered yet (23).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Insulin Receptor Substrate 1 (IRS1) Promotes Radioresistance in A172 Glioblastoma Cell Line

Görgişen¹,

Çakır²,

Ateş³

et al. 2019

Eastern J Med

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Insulin receptor substrate 1 (IRS1) is the main adaptor molecule in insulin and insulin like growth factor signaling. Increased level of expression of IRS1 and IGF-1R proteins are associated with many human malignancies. They also induced resistance to therapeutic approaches such as chemo-and radiotherapy in cancer treatment however their molecular mechanisms are still unclear. Glioblastoma Multiforme (GBM) is the most common primary brain tumor in adults and radiotherapy has a pivotal role in its treatment. In this study, it is aimed to determine the relationship between IRS1 expression and radiosensitivity of GBM cells. Therefore, A172 cells transfected with pcDNA3.1-HA-tagged human IRS1 gene. Its overexpression was confirmed by western blot. IRS1 overexpressed A172 cells were irradiated with 5,8 and 10 Gray ionizing radiation and their effects on cell viability determined by MTT and clonogenic assay. Our results showed that overexpression of IRS1 led a decrease on sensitivity of the radiation in GBM cel ls. As a conclusion, this study should be confirmed by further molecular analysis and in vivo studies. IRS1 may be a predictive marker of radiosensitivity for GBM.

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MicroRNA-1225-5p behaves as a tumor suppressor in human glioblastoma via targeting of IRS1

Cited by 21 publications

References 37 publications

MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

MiR-1225-5p acts as tumor suppressor in glioblastoma via targeting FNDC3B

<p>MicroRNA-559 plays an inhibitory role in the malignant progression of glioblastoma cells by directly targeting metadherin</p>

Overexpression of Insulin Receptor Substrate 1 (IRS1) Promotes Radioresistance in A172 Glioblastoma Cell Line

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