scholarly journals Role of the Mammalian Target of Rapamycin Pathway in Liver Cancer: From Molecular Genetics to Targeted Therapies

Hepatology ◽  
2020 ◽  
Author(s):  
Xinjun Lu ◽  
Panagiotis Paliogiannis ◽  
Diego F. Calvisi ◽  
Xin Chen
Keyword(s):  
Liver Cancer ◽  
Molecular Genetics ◽  
Targeted Therapies ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin

scholarly journals Role of mammalian target of rapamycin complex 2 in primary and secondary liver cancer

2021 ◽  
Vol 13 (11) ◽  
pp. 1632-1647
Author(s):  
Katharina Joechle ◽  
Jessica Guenzle ◽  
Claus Hellerbrand ◽  
Pavel Strnad ◽  
Thorsten Cramer ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin

Role of mTOR1 and mTOR2 complexes in MEG-01 cell physiology

2015 ◽  
Vol 114 (11) ◽  
pp. 969-981 ◽  
Author(s):  
Esther López ◽  
Alejandro Berna-Erro ◽  
Javier J. López ◽  
María P. Granados ◽  
Nuria Bermejo ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Cell Physiology ◽  
Cell Stimulation ◽  
Intracellular Location ◽  
Macromolecular Complexes

SummaryThe function of the mammalian target of rapamycin (mTOR) is upregulated in response to cell stimulation with growing and differentiating factors. Active mTOR controls cell proliferation, differentiation and death. Since mTOR associates with different proteins to form two functional macromolecular complexes, we aimed to investigate the role of the mTORI and mTOR2 complexes in MEG-01 cell physiology in response to thrombopoietin (TPO). By using mTOR antagonists and overexpressing FKBP38, we have explored the role of both mTOR complexes in proliferation, apoptosis, maturation-like mechanisms, endoplasmic reticulum-stress and the intracellular location of both active mTOR complexes during MEG-01 cell stimulation with TPO. The results demonstrate that mTOR1 and mTOR2 complexes play different roles in the physiology of MEG-01 cells and in the maturation-like mechanisms; hence, these findings might help to understand the mechanism underlying generation of platelets.

Role of Mammalian Target of Rapamycin in Muscle Growth

2019 ◽  
pp. 251-261
Author(s):  
Evgeniy Panzhinskiy ◽  
Bruce Culver ◽  
Jun Ren ◽  
Debasis Bagchi ◽  
Sreejayan Nair
Keyword(s):  
Muscle Growth ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin

scholarly journals The Role of Mammalian Target of Rapamycin in Hypertensive Rat Atria

2011 ◽  
Vol 27 (Supplement) ◽  
pp. OP04_2
Author(s):  
Koichi Nagashima ◽  
Takeshi Yamashita ◽  
Akiko Sekiguchi ◽  
Ichiro Watanabe ◽  
Atsushi Hirayama
Keyword(s):  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Rat Atria ◽  
Hypertensive Rat

scholarly journals Profiling the Role of Mammalian Target of Rapamycin in the Vascular Smooth Muscle Metabolome in Pulmonary Arterial Hypertension

2015 ◽  
Vol 5 (4) ◽  
pp. 667-680 ◽  
Author(s):  
Tatiana V. Kudryashova ◽  
Dmitry A. Goncharov ◽  
Andressa Pena ◽  
Kaori Ihida-Stansbury ◽  
Horace DeLisser ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Arterial Hypertension ◽  
Vascular Smooth Muscle ◽  
Arterial Hypertension ◽  
Mammalian Target Of Rapamycin ◽  
Target Of Rapamycin ◽  
Pulmonary Arterial

scholarly journals Minireview: Lymphangioleiomyomatosis (LAM): The “Other” Steroid-Sensitive Cancer

Endocrinology ◽  
2016 ◽  
Vol 157 (9) ◽  
pp. 3374-3383 ◽  
Author(s):  
Hen Prizant ◽  
Stephen R. Hammes
Keyword(s):  
Sexual Dimorphism ◽  
Mammalian Target Of Rapamycin ◽  
Progesterone Receptors ◽  
Basic Research ◽  
Target Of Rapamycin ◽  
Childbearing Age ◽  
Genes Encoding ◽  
Childbearing Age Women ◽  
Steroid Sensitive

Lymphangioleiomyomatosis (LAM) is a devastating rare lung disease affecting primarily childbearing age women in which tumors consisting of abnormal smooth-muscle-like cells grow within the lungs and progressively lead to loss of pulmonary function. LAM cells metastasize to the lungs, predominantly through the lymphatics; however, the source of the LAM cell is still unknown. LAM cells contain inactivating mutations in genes encoding tuberous sclerosis 1 or 2, proteins that normally limit cell growth through suppression of mammalian target of rapamycin complex 1. As of today, sirolimus (an mammalian target of rapamycin complex 1 inhibitor) is the only treatment, available for LAM patients that is approved by the Food and Drug Administration; however, this drug and others in its class provide stabilization but not remission of LAM. One of the biggest problems in treating LAM is that both the origin of the LAM cells and the mechanism of the sexual dimorphism in LAM are still not understood. LAM cells express estrogen and progesterone receptors, and lung function declines during periods of high circulating estrogen levels. Moreover, numerous basic research studies find that estrogen is a key driving force in LAM cell proliferation, migration, and metastasis. In this review, we highlight recent insights regarding the role of steroid hormones in LAM and discuss possible explanations for the profound female sexual dimorphism of LAM.

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