Roles of mTOR Signaling in Tissue Regeneration

Wei, Xiangyong; Luo, Lingfei; Chen, Jinzi

doi:10.3390/cells8091075

Cited by 97 publications

(72 citation statements)

References 229 publications

(299 reference statements)

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“…Moreover, GSK-3 participates in the regulation of glycogen metabolism by mediating glycogen synthesis, glucose transport, liver gluconeogenesis and beta cell function [53,54]. mTOR mTOR, a serine/threonine protein kinase, is a member of the PI3K-associated kinase protein family that participates in sensing nutritional signals and regulating cell growth and proliferation [55]. mTOR includes mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2).…”

Section: Akt Target Proteinsmentioning

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RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours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

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RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours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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“…Furthermore, p70 S6 kinase is also required for cell growth and cell cycle progression under normal physiologic conditions [39]. On the contrary, the abnormal activation of mTOR and p70S6K kinases has been reported as dictating cancer development in various human tumors [40]. Therefore, targeting of the mTOR/p70S6K pathway is becoming an attractive therapeutic strategy for cancer treatment [41,42].…”

Section: Discussionmentioning

confidence: 99%

ZnO Nanoparticles Induced Caspase-Dependent Apoptosis in Gingival Squamous Cell Carcinoma through Mitochondrial Dysfunction and p70S6K Signaling Pathway

Wang

Lee

Lin

et al. 2020

IJMS

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Zinc oxide nanoparticles (ZnO-NPs) are increasingly used in sunscreens, food additives, pigments, rubber manufacture, and electronic materials. Several studies have shown that ZnO-NPs inhibit cell growth and induce apoptosis by the production of oxidative stress in a variety of human cancer cells. However, the anti-cancer property and molecular mechanism of ZnO-NPs in human gingival squamous cell carcinoma (GSCC) are not fully understood. In this study, we found that ZnO-NPs induced growth inhibition of GSCC (Ca9-22 and OECM-1 cells), but no damage in human normal keratinocytes (HaCaT cells) and gingival fibroblasts (HGF-1 cells). ZnO-NPs caused apoptotic cell death of GSCC in a concentration-dependent manner by the quantitative assessment of oligonucleosomal DNA fragmentation. Flow cytometric analysis of cell cycle progression revealed that sub-G1 phase accumulation was dramatically induced by ZnO-NPs. In addition, ZnO-NPs increased the intracellular reactive oxygen species and specifically superoxide levels, and also decreased the mitochondrial membrane potential. ZnO-NPs further activated apoptotic cell death via the caspase cascades. Importantly, anti-oxidant and caspase inhibitor clearly prevented ZnO-NP-induced cell death, indicating the fact that superoxide-induced mitochondrial dysfunction is associated with the ZnO-NP-mediated caspase-dependent apoptosis in human GSCC. Moreover, ZnO-NPs significantly inhibited the phosphorylation of ribosomal protein S6 kinase (p70S6K kinase). In a corollary in vivo study, our results demonstrated that ZnO-NPs possessed an anti-cancer effect in a zebrafish xenograft model. Collectively, these results suggest that ZnO-NPs induce apoptosis through the mitochondrial oxidative damage and p70S6K signaling pathway in human GSCC. The present study may provide an experimental basis for ZnO-NPs to be considered as a promising novel anti-tumor agent for the treatment of gingival cancer.

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“…Glial scars, formed by the activation of inactive astrocytes, involve the proliferation or hypertrophy of astrocytes, which create a physical and chemical barrier that hinders neuronal recovery [40]. The conversion of astrocytes depends on epidermal growth factors (EGF), which activates the Rheb/mTOR pathway [5]. Overexpressed PTEN attenuates gliosis at three days after SCI and enhances motor functional recovery [5] (Figure 3b).…”

Section: The Cell-specific Mtor Signaling Roles In Mammalian Spinal Cmentioning

confidence: 99%

“…Raptor and Rictor protein scaffolds participate in assembling the different constituents of the complexes and binding substrates. Detailed data about the structure, components and regulation of both TORC1 and TORC2 complexes are available in several recent reviews [3][4][5]. S6K1/2 (S6 kinase 1/2) and 4E-BP (4E binding protein) constitute important substrates phosphorylated by the serine/threonine kinase TOR to initiate protein translation and are commonly used as readout for TORC activity.…”

Section: Introductionmentioning

confidence: 99%

mTOR Signaling at the Crossroad between Metazoan Regeneration and Human Diseases

Lund-Ricard

Morales

Boutet

2020

IJMS

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A major challenge in medical research resides in controlling the molecular processes of tissue regeneration, as organ and structure damage are central to several human diseases. A survey of the literature reveals that mTOR (mechanistic/mammalian target of rapamycin) is involved in a wide range of regeneration mechanisms in the animal kingdom. More particularly, cellular processes such as growth, proliferation, and differentiation are controlled by mTOR. In addition, autophagy, stem cell maintenance or the newly described intermediate quiescence state, Galert, imply upstream monitoring by the mTOR pathway. In this review, we report the role of mTOR signaling in reparative regenerations in different tissues and body parts (e.g., axon, skeletal muscle, liver, epithelia, appendages, kidney, and whole-body), and highlight how the mTOR kinase can be viewed as a therapeutic target to boost organ repair. Studies in this area have focused on modulating the mTOR pathway in various animal models to elucidate its contribution to regeneration. The diversity of metazoan species used to identify the implication of this pathway might then serve applied medicine (in better understanding what is required for efficient treatments in human diseases) but also evolutionary biology. Indeed, species-specific differences in mTOR modulation can contain the keys to appreciate why certain regeneration processes have been lost or conserved in the animal kingdom.

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Roles of mTOR Signaling in Tissue Regeneration

Cited by 97 publications

References 229 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

ZnO Nanoparticles Induced Caspase-Dependent Apoptosis in Gingival Squamous Cell Carcinoma through Mitochondrial Dysfunction and p70S6K Signaling Pathway

mTOR Signaling at the Crossroad between Metazoan Regeneration and Human Diseases

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