TOR kinase complexes and cell migration

Liu, Lunhua; Parent, Carole A.

doi:10.1083/jcb.201102090

Cited by 80 publications

(62 citation statements)

References 140 publications

(210 reference statements)

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“…Recent studies have shown that mTOR also plays a critical role in the regulation of tumor cell motility, invasion, and cancer metastasis (41). However, the role of GOLPH3 in cancer cell migration and metastasis remains largely unknown.…”

Section: Expression Of Golph3 Is Important For Integrin-meditatedmentioning

confidence: 99%

An Oncogenic Protein Golgi Phosphoprotein 3 Up-regulates Cell Migration via Sialylation

Isaji

et al. 2014

Journal of Biological Chemistry

133

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Background: Molecular mechanisms of the effect of the GOLPH3 oncogenic protein on tumorigenesis remain unclear. Results: GOLPH3 specifically up-regulates sialylation of integrin N-glycans, promotes sialylation-dependent cell migration, and affects AKT signaling. Conclusion: GOLPH3 affects cell biological functions through a specific regulation of sialylation. Significance: The sialylation of N-glycans is important for functions of GOLPH3.

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Section: Expression Of Golph3 Is Important For Integrin-meditatedmentioning

confidence: 99%

An Oncogenic Protein Golgi Phosphoprotein 3 Up-regulates Cell Migration via Sialylation

Isaji

et al. 2014

Journal of Biological Chemistry

133

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“…Circulating naive neutrophils are apolar, but upon stimulation by chemoattractants they rapidly polarize in a manner that is epitomized by formation of lamellar-type F actin at the front and localization of active RHOA and phosphorylated myosin light chain (pMLC, also known as MYL2) at the back (Bourne and Weiner, 2002;Graziano and Weiner, 2014;Liu and Parent, 2011;Wang, 2009;Wu, 2005). It remains, however, incompletely understood how RHOA activation and pMLC localization is polarized.…”

Section: Introductionmentioning

confidence: 99%

Front Signal-Dependent Accumulation of RHOA Inhibitor FAM65B at Leading Edges Polarizes Neutrophils

Gao

Tang

et al. 2015

Journal of Cell Science

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A hallmark of neutrophil polarization is the back localization of active RHOA and phosphorylated myosin light chain (pMLC, also known as MYL2). However, the mechanism for the polarization is not entirely clear. Here, we show that FAM65B, a newly identified RHOA inhibitor, is important for the polarization. When FAM65B is phosphorylated, it binds to 14-3-3 family proteins and becomes more stable. In neutrophils, chemoattractants stimulate FAM65B phosphorylation largely depending on the signals from the front of the cells that include those mediated by phospholipase Cb (PLCb) and phosphoinositide 3-kinase c (PI3Kc), leading to FAM65B accumulation at the leading edge. Concordantly, FAM65B deficiency in neutrophils resulted in an increase in RHOA activity and localization of pMLC to the front of cells, as well as defects in chemotaxis directionality and adhesion to endothelial cells under flow. These data together elucidate a mechanism for RHOA and pMLC polarization in stimulated neutrophils through direct inhibition of RHOA by FAM65B at the leading edge.

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“…As a serine/threonine protein kinase, mTOR mediates growth factor–induced cell migration 62. mTOR inhibitors were clinically approved to reduce restenosis after angioplasty for patients with vascular occlusion 63, 64.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of 5‐Hydroxytryptamine Receptor 2B Reduced Vascular Restenosis and Mitigated the β‐Arrestin2–Mammalian Target of Rapamycin/p70S6K Pathway

Liu

Wang

et al. 2018

JAHA

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BackgroundAs a monoamine neurotransmitter, 5‐hydroxytryptamine (5‐HT) or serotonin modulates mood, appetite, and sleep. Besides, 5‐HT also has important peripheral functions. 5‐HT receptor 2B (5‐HT2BR) plays a key role in cardiovascular diseases, such as pulmonary arterial hypertension and cardiac valve disease. Percutaneous intervention has been used to restore blood flow in occlusive vascular disease. However, restenosis remains a significant problem. Herein, we investigated the role of 5‐HT2BR in neointimal hyperplasia, a key pathological process in restenosis.Methods and ResultsThe expression of 5‐HT2BR was upregulated in wire‐injured mouse femoral arteries. In addition, BW723C86, a selective 5‐HT2BR agonist, promoted the injury response during restenosis. 5‐HT and BW723C86 stimulated migration and proliferation of rat aortic smooth muscle cells. Conversely, LY272015, a selective antagonist, attenuated the 5‐HT–induced smooth muscle cell migration and proliferation. In vitro study showed that the promigratory effects of 5‐HT2BR were mediated through the activation of mammalian target of rapamycin (mTOR)/p70S6K signaling in a β‐arrestin2–dependent manner. Inhibition of mammalian target of rapamycin or p70S6K mitigated 5‐HT2BR–mediated smooth muscle cell migration. Mice with deficiency of 5‐HT2BR showed significantly reduced neointimal formation in wire‐injured arteries.ConclusionsThese results demonstrated that activation of 5‐HT2BR and β‐arrestin2–biased downstream signaling are key pathological processes in neointimal formation, and 5‐HT2BR may be a potential target for the therapeutic intervention of vascular restenosis.

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TOR kinase complexes and cell migration

Cited by 80 publications

References 140 publications

An Oncogenic Protein Golgi Phosphoprotein 3 Up-regulates Cell Migration via Sialylation

An Oncogenic Protein Golgi Phosphoprotein 3 Up-regulates Cell Migration via Sialylation

Front Signal-Dependent Accumulation of RHOA Inhibitor FAM65B at Leading Edges Polarizes Neutrophils

Inhibition of 5‐Hydroxytryptamine Receptor 2B Reduced Vascular Restenosis and Mitigated the β‐Arrestin2–Mammalian Target of Rapamycin/p70S6K Pathway

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