Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme

Tuncel, Gülten; Kalkan, Rasime

doi:10.1007/s12032-018-1185-5

Cited by 22 publications

(15 citation statements)

References 98 publications

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“…AKT is regulated by a variety of hormones, including insulin and growth factors [26]. As mentioned above, after the PI3K regulatory subunit binds to the corresponding receptors or receptor-binding protein on the cell membrane, its catalytic subunit is activated and catalyses the formation of PIP3, which then recruits PDK1 and AKT to the cell membrane [26,27].…”

Section: Aktmentioning

confidence: 99%

RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

et al. 2020

Cell Biosci

469

263

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The PI3 K/AKT/mTOR signalling pathway plays an important role in the regulation of signal transduction and biological processes such as cell proliferation, apoptosis, metabolism and angiogenesis. Compared with those of other signalling pathways, the components of the PI3K/AKT/mTOR signalling pathway are complicated. The regulatory mechanisms and biological functions of the PI3K/AKT/mTOR signalling pathway are important in many human diseases, including ischaemic brain injury, neurodegenerative diseases, and tumours. PI3K/AKT/mTOR signalling pathway inhibitors include single-component and dual inhibitors. Numerous PI3K inhibitors have exhibited good results in preclinical studies, and some have been clinically tested in haematologic malignancies and solid tumours. In this review, we briefly summarize the results of research on the PI3K/AKT/mTOR pathway and discuss the structural composition, activation, communication processes, regulatory mechanisms and biological functions of the PI3K/AKT/mTOR signalling pathway in the pathogenesis of neurodegenerative diseases and tumours.

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Section: Aktmentioning

confidence: 99%

RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

et al. 2020

Cell Biosci

469

263

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“…Ras is a key effector that activates downstream signaling cascades when phosphorylated (Tuncel and Kalkan, 2018). As shown in Figure 6, phosphorylation of Ras was significantly increased in the DSS group compared to that in the control group (p < 0.01).…”

Section: Huangqin Decoction Attenuated Inflammation Through Inhibitiomentioning

confidence: 89%

Anti-Inflammatory Effects of Huangqin Decoction on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through Regulation of the Gut Microbiota and Suppression of the Ras-PI3K-Akt-HIF-1α and NF-κB Pathways

Luo

et al. 2020

Front. Pharmacol.

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Objective: Huangqin decoction (HQD), a classical traditional Chinese medicinal formula, has been commonly used to treat gastrointestinal diseases for thousands of years. We investigated the anti-inflammatory effects and underlying mechanisms of HQD on dextran sulfate sodium (DSS)-induced ulcerative colitis (UC).Methods: Experimental mice were given 3% DSS, and HQD (2.275, 4.55, and 9.1 g/kg), or mesalazine (ME, 200 mg/kg) orally for 7 days. Body weight loss, disease activity index (DAI), colon length, histology, and levels of inflammatory cytokines were measured to evaluate the effects of HQD on colitis. The effects of HQD on the Ras-phosphoinositide-3kinase (PI3K)-Akt-hypoxia inducible factor 1 alpha (HIF-1a) and nuclear factor-kappa B (NF-kB) pathways were evaluated by Western blot analysis. In addition, the gut microbiota was characterized using high-throughput Illumina MiSeq sequencing. Results:The results showed that HQD significantly reduced the body weight loss, ameliorated DAI, restored colon length, and improved the intestinal epithelial cell barrier in mice with DSS-induced colitis. The messenger RNA (mRNA) expression levels of inflammatory mediators were decreased following HQD treatment. Furthermore, the Ras-PI3K-Akt-HIF-1a and NF-kB pathways were significantly inhibited by HQD. Finally, treatment with HQD resulted in recovery of gut microbiota diversity.Conclusions: HQD ameliorates DSS-induced colitis through regulation of the gut microbiota, and suppression of Ras-PI3K-Akt-HIF-1a and NF-kB pathways. Our results suggested that HQD may be a potential candidate for treatment of UC.GRAPHICAL ABSTRACT | This study demonstrated that supplementation of Huangqin decoction (HQD) attenuated dextran sulfate sodium (DSS)-induced ulcerative colitis by regulating the gut microbiota and suppressing Ras-PI3K-Akt-HIF-1a and NF-kB pathways in mice.

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“…The EGFR, also known as ErbB1/Her1 [55], is a key factor for brain tumors as it supports the proliferation and stemness of neural progenitor cells from which these tumors originate. Upon EGF binding, the EGFR undergoes conformational changes and autophosphorylation, thus favoring the binding of the regulatory subunit of PI3K and activation of a signaling cascade that leads to phosphorylation and activation of AKT [56]. In turn, the PI3K/AKT pathway plays a pivotal role in the regulation of key biological processes in brain tumors, including cell proliferation, metabolism, survival, migration and angiogenesis [57].…”

Section: Egfr Signaling Pathwaymentioning

confidence: 99%

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

Bielli

Pagliarini

Pieraccioli

et al. 2019

Cells

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Brain tumors are a heterogeneous group of neoplasms ranging from almost benign to highly aggressive phenotypes. The malignancy of these tumors mostly relies on gene expression reprogramming, which is frequently accompanied by the aberrant regulation of RNA processing mechanisms. In brain tumors, defects in alternative splicing result either from the dysregulation of expression and activity of splicing factors, or from mutations in the genes encoding splicing machinery components. Aberrant splicing regulation can generate dysfunctional proteins that lead to modification of fundamental physiological cellular processes, thus contributing to the development or progression of brain tumors. Herein, we summarize the current knowledge on splicing abnormalities in brain tumors and how these alterations contribute to the disease by sustaining proliferative signaling, escaping growth suppressors, or establishing a tumor microenvironment that fosters angiogenesis and intercellular communications. Lastly, we review recent efforts aimed at developing novel splicing-targeted cancer therapies, which employ oligonucleotide-based approaches or chemical modulators of alternative splicing that elicit an impact on brain tumor biology.

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Receptor tyrosine kinase-Ras-PI 3 kinase-Akt signaling network in glioblastoma multiforme

Cited by 22 publications

References 98 publications

RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

Anti-Inflammatory Effects of Huangqin Decoction on Dextran Sulfate Sodium-Induced Ulcerative Colitis in Mice Through Regulation of the Gut Microbiota and Suppression of the Ras-PI3K-Akt-HIF-1α and NF-κB Pathways

Splicing Dysregulation as Oncogenic Driver and Passenger Factor in Brain Tumors

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