Involvement of mTORC1 and mTORC2 in regulation of glioblastoma multiforme growth and motility

Gulati, Nicholas; Karsy, Michael; Albert, Ladislau; Murali, Raj; Jhanwar‐Uniyal, Meena

doi:10.3892/ijo_00000386

Cited by 31 publications

(9 citation statements)

References 40 publications

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“…The use of inhibitors of STAT3 upstream regulators pointed that STAT3 might be involved in glioma cell migration and invasion [173,174,177,178]. This inhibition of STAT3 has been linked to down-regulation of matrix metalloproteinase gene expression such as MMP2 [179], MMP9 and to epithelial-mesenchymal transition regulating genes like Snail [180] (Figure 3).…”

Section: Stat3 Activation Role In Glioma Cell Migration and Invasionmentioning

confidence: 99%

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

et al. 2016

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Signal transducer and activator of transcription 3 (STAT3) is aberrantly activated in glioblastoma and has been identified as a relevant therapeutic target in this disease and many other human cancers. After two decades of intensive research, there is not yet any approved STAT3-based glioma therapy. In addition to the canonical activation by tyrosine 705 phosphorylation, concordant reports described a potential therapeutic relevance of other post-translational modifications including mainly serine 727 phosphorylation. Such reports reinforce the need to refine the strategy of targeting STAT3 in each concerned disease. This review focuses on the role of serine 727 and tyrosine 705 phosphorylation of STAT3 in glioma. It explores their contribution to glial cell transformation and to the mechanisms that make glioma escape to both immune control and standard treatment.

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Section: Stat3 Activation Role In Glioma Cell Migration and Invasionmentioning

confidence: 99%

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

et al. 2016

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“…In addition, some environmental carcinogenic factors may also be associated with the occurrence of glioma. Research has shown that electromagnetic radiation, such as mobile phone use, may be related to glioma [8]. In addition, most glioblastoma patients also have cytomegalovirus infection, and most glioblastoma specimens were found to contain virally infected macrophages [9].…”

Section: Introductionmentioning

confidence: 99%

Upregulation of miR-184 Enhances the Malignant Biological Behavior of Human Glioma Cell Line A172 by Targeting FIH-1

Yuan

Gao

Liu

et al. 2014

Cell Physiol Biochem

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Background: In recent years, miRNAs have been suggested to play key roles in the formation and development of human glioma. The aim of this study is to investigate the effect and mechanism of miR-184 expression on the malignant behavior of human glioma cells. Methods: The relative quantity of miR-184 was determined in human glioma cell lines, and the expression of hypoxia-inducible factor-1 alpha (HIF-1α) was explored using western blotting. The effects of miR-184 inhibition on cell viability and apoptosis were explored, and the miR-184 target gene was determined using a luciferase assay and western blotting. Flow cytometry and Hoechst staining were used to evaluate cell growth and apoptosis. Matrigel invasion and scratch assays were performed to measure the ability of cell invasion and migration. Results: miR-184 and HIF-1α protein levels were significantly upregulated in human glioma cells. Downregulation of miR-184 inhibited cell viability and increased the HEB cell apoptotic rate. Luciferase and western blot assays verified that FIH-1 was the target gene of miR-184 and negatively controlled the protein level of HIF-1α. Inhibition of HIF-1α by siRNA facilitated the apoptosis of HEB cells and suppressed A172 cell invasion and migration. Conclusion: miR-184 upregulation enhanced the malignant phenotype of human glioma cancer cells by reducing FIH-1 protein expression.

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“…In PI3K signaling cascade, mTOR acts like downstream effector molecule as well as an upstream modulator [ 40 ]. It resides in mTORC1 and mTORC2 [ 41 ]. The mTORC1 consists of mTOR, mLST8, PRAS40 and Raptor.…”

Section: Underlying Mechanisms For Gbm Progressmentioning

confidence: 99%

Current Perspective on the Natural Compounds and Drug Delivery Techniques in Glioblastoma Multiforme

Behl

Sharma

et al. 2021

Cancers

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Glioblastoma multiforme (GBM) is one of the debilitating brain tumors, being associated with extremely poor prognosis and short median patient survival. GBM is associated with complex pathogenesis with alterations in various cellular signaling events, that participate in cell proliferation and survival. The impairment in cellular redox pathways leads to tumorigenesis. The current standard pharmacological regimen available for glioblastomas, such as radiotherapy and surgical resection following treatment with chemotherapeutic drug temozolomide, remains fatal, due to drug resistance, metastasis and tumor recurrence. Thus, the demand for an effective therapeutic strategy for GBM remains elusive. Hopefully, novel products from natural compounds are suggested as possible solutions. They protect glial cells by reducing oxidative stress and neuroinflammation, inhibiting proliferation, inducing apoptosis, inhibiting pro-oncogene events and intensifying the potent anti-tumor therapies. Targeting aberrant cellular pathways in the amelioration of GBM could promote the development of new therapeutic options that improve patient quality of life and extend survival. Consequently, our review emphasizes several natural compounds in GBM treatment. We also assessed the potential of drug delivery techniques such as nanoparticles, Gliadel wafers and drug delivery using cellular carriers which could lead to a novel path for the obliteration of GBM.

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Involvement of mTORC1 and mTORC2 in regulation of glioblastoma multiforme growth and motility

Cited by 31 publications

References 40 publications

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

Role of STAT3 in Genesis and Progression of Human Malignant Gliomas

Upregulation of miR-184 Enhances the Malignant Biological Behavior of Human Glioma Cell Line A172 by Targeting FIH-1

Current Perspective on the Natural Compounds and Drug Delivery Techniques in Glioblastoma Multiforme

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