scholarly journals C16‑ceramide and sphingosine�1‑phosphate/S1PR2 have opposite effects on cell growth through mTOR signaling pathway regulation

2018 ◽  
Author(s):  
Min Kim ◽  
Joo‑Won Park ◽  
Eun‑Ji Lee ◽  
Shin Kim ◽  
Sun‑Hye Shin ◽  
...  
Keyword(s):  
Cell Growth ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Sphingosine 1 Phosphate ◽  
Pathway Regulation

scholarly journals Downregulation of BZW2 inhibits osteosarcoma cell growth by inactivating the Akt/mTOR signaling pathway

2017 ◽  
Vol 38 (4) ◽  
pp. 2116-2122 ◽  
Author(s):  
Dong-Dong Cheng ◽  
Shi-Jie Li ◽  
Bin Zhu ◽  
Ting Yuan ◽  
Qing-Cheng Yang ◽  
...  
Keyword(s):  
Cell Growth ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Osteosarcoma Cell ◽  
Mtor Signaling Pathway

scholarly journals Transcriptome profiling of the newborn mouse lung after hypoxia and reoxygenation: hyperoxic reoxygenation affects mTOR signaling pathway, DNA repair, and JNK-pathway regulation

2013 ◽  
Vol 74 (5) ◽  
pp. 536-544 ◽  
Author(s):  
Embjørg J. Wollen ◽  
Yngve Sejersted ◽  
Marianne S. Wright ◽  
Miroslaw Bik-Multanowski ◽  
Anna Madetko-Talowska ◽  
...  
Keyword(s):  
Dna Repair ◽  
Signaling Pathway ◽  
Transcriptome Profiling ◽  
Mtor Signaling ◽  
Mouse Lung ◽  
Newborn Mouse ◽  
Mtor Signaling Pathway ◽  
Jnk Pathway ◽  
Pathway Regulation

Novel Gemini-vitamin D3 analog inhibits tumor cell growth and modulates the Akt/mTOR signaling pathway

2006 ◽  
Vol 100 (4-5) ◽  
pp. 107-116 ◽  
Author(s):  
James O’Kelly ◽  
Milan Uskokovic ◽  
Nathan Lemp ◽  
Jay Vadgama ◽  
H. Phillip Koeffler
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Signaling Pathway ◽  
Vitamin D3 ◽  
Mtor Signaling ◽  
Tumor Cell Growth ◽  
Mtor Signaling Pathway

scholarly journals Is REDD1 a metabolic double agent? Lessons from physiology and pathology

2020 ◽  
Vol 319 (5) ◽  
pp. C807-C824
Author(s):  
Florian A. Britto ◽  
Karine Dumas ◽  
Sophie Giorgetti-Peraldi ◽  
Vincent Ollendorff ◽  
François B. Favier
Keyword(s):  
Cell Growth ◽  
Signaling Pathway ◽  
Inflammatory Diseases ◽  
Mtor Signaling ◽  
Metabolic Adaptation ◽  
Mtor Signaling Pathway ◽  
Regulate Cell Growth ◽  
Early Biomarker ◽  
Double Agent ◽  
Metabolic Stresses

The Akt/mechanistic target of rapamycin (mTOR) signaling pathway governs macromolecule synthesis, cell growth, and metabolism in response to nutrients and growth factors. Regulated in development and DNA damage response (REDD)1 is a conserved and ubiquitous protein, which is transiently induced in response to multiple stimuli. Acting like an endogenous inhibitor of the Akt/mTOR signaling pathway, REDD1 protein has been shown to regulate cell growth, mitochondrial function, oxidative stress, and apoptosis. Recent studies also indicate that timely REDD1 expression limits Akt/mTOR-dependent synthesis processes to spare energy during metabolic stresses, avoiding energy collapse and detrimental consequences. In contrast to this beneficial role for metabolic adaptation, REDD1 chronic expression appears involved in the pathogenesis of several diseases. Indeed, REDD1 expression is found as an early biomarker in many pathologies including inflammatory diseases, cancer, neurodegenerative disorders, depression, diabetes, and obesity. Moreover, prolonged REDD1 expression is associated with cell apoptosis, excessive reactive oxygen species (ROS) production, and inflammation activation leading to tissue damage. In this review, we decipher several mechanisms that make REDD1 a likely metabolic double agent depending on its duration of expression in different physiological and pathological contexts. We also discuss the role played by REDD1 in the cross talk between the Akt/mTOR signaling pathway and the energetic metabolism.

scholarly journals Hypoxia-Related Gene FUT11 Promotes Pancreatic Cancer Progression by Maintaining the Stability of PDK1

2021 ◽  
Vol 11 ◽  
Author(s):  
Wenpeng Cao ◽  
Zhirui Zeng ◽  
Runsang Pan ◽  
Hao Wu ◽  
Xiangyan Zhang ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Growth ◽  
Western Blot ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Cell Growth And Migration ◽  
And Migration ◽  
The Stability

BackgroundHypoxia is associated with the development of pancreatic cancer (PC). However, genes associated with hypoxia response and their regulatory mechanism in PC cells were unclear. The current study aims to investigate the role of the hypoxia associated gene fucosyltransferase 11 (FUT11) in the progression of PC.MethodsIn the preliminary study, bioinformatics analysis predicted FUT11 as a key hypoxia associated gene in PC. The expression of FUT11 in PC was evaluated using quantitative real-time PCR (qRT-PCR), Western blot and immunohistochemistry. The effects of FUT11 on PC cells proliferation and migration under normoxia and hypoxia were evaluated using Cell Counting Kit 8, 5-ethynyl-2’-deoxyuridine (EDU) assay, colony formation assay and transwell assay. The effects of FUT11 in vivo was examined in mouse tumor models of liver metastasis and subcutaneous xenograft. Furthermore, Western blot, luciferase assay and immunoprecipitation were performed to explore the regulatory relationship among FUT11, hypoxia-inducible factor 1α (HIF1α) and pyruvate dehydrogenase kinase 1 (PDK1) in PC.ResultsFUT11 was markedly increased of PC cells with hypoxia, upregulated in the PC clinical tissues, and predicted a poor outcome of PC patients. Inhibition of FUT11 reduced PC cell growth and migratory ability of PC cells under normoxia and hypoxia conditions in vitro, and growth and tumor cell metastasis in vivo. FUT11 bound to PDK1 and regulated the expression PDK1 under normoxia and hypoxia. FUT11 interacted with PDK1 and decreased the ubiquitination of PDK1, lead to the activation of AKT/mTOR signaling pathway. FUT11 knockdown significantly increased the degradation of PDK1 under hypoxia, while treatment with MG132 can relieve the degradation of PDK1 induced by FUT11 knockdown. Overexpression of PDK1 in PC cells under hypoxia conditions reversed the suppressive impacts of FUT11 knockdown on PC cell growth and migration. In addition, HIF1α bound to the promoter of FUT11 and increased its expression, as well as co-expressed with FUT11 in PC tissues. Furthermore, overexpression of FUT11 partially rescued the suppressive effects of HIF1α knockdown on PC cell growth and migration in hypoxia condition.ConclusionOur data implicate that hypoxia-induced FUT11 contributes to proliferation and metastasis of PC by maintaining the stability of PDK1, thus mediating activation of AKT/mTOR signaling pathway, and suggest that FUT11 could be a novel and effective target for the treatment of pancreatic cancer.

scholarly journals Betaine alleviates alcohol-induced osteonecrosis of the femoral head via mTOR signaling pathway regulation

2019 ◽  
Vol 120 ◽  
pp. 109486 ◽  
Author(s):  
Qianhao Yang ◽  
Wenjing Yin ◽  
Yixuan Chen ◽  
Daoyu Zhu ◽  
Junhui Yin ◽  
...  
Keyword(s):  
Femoral Head ◽  
Signaling Pathway ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway ◽  
Pathway Regulation
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