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1.
Int J Oncol ; 53(5): 1827-1835, 2018 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-30106141

RESUMO

The novel neurite outgrowth inhibitor B (Nogo­B) receptor (NgBR) is specific for Nogo­B, which is highly expressed in various human organs and cells, including the lung, liver, kidney, smooth muscle cells, blood vessel endothelial cells and inflammatory cells. Previous studies have indicated that NgBR directly interacts with Nogo­B and is able to independently influence lipid and cholesterol homeostasis, angiogenesis, N­glycosylation, the epithelial-mesenchymal transition, the chemotaxis of endothelial cells and cellular proliferation and apoptosis. These multiple functions and actions of this receptor provide an understanding of the important roles of NgBR in various conditions, including fatty liver, atherosclerosis, intracranial microaneurysms, retinitis pigmentosa and severe neurological impairment. Furthermore, NgBR has been demonstrated to exert protean, multifunctional and enigmatic effects in cancer. The present review summarizes the latest knowledge on the suppressing and activating effects of NgBR, emphasizing its function in cancer. Further basic and medical research on this receptor may provide novel insight into its clinical implications on the prognosis of relevant human cancer types.


Assuntos
Transição Epitelial-Mesenquimal/fisiologia , Neoplasias/genética , Receptores de Superfície Celular/genética , Receptores de Superfície Celular/metabolismo , Proteínas Quinases Ativadas por AMP/metabolismo , Animais , Estresse do Retículo Endoplasmático , Regulação Neoplásica da Expressão Gênica , Glicosilação , Humanos , Metabolismo dos Lipídeos , Receptores X do Fígado/metabolismo , Neoplasias/patologia , Neovascularização Patológica/etiologia , Proteínas Proto-Oncogênicas c-akt/metabolismo , Resposta a Proteínas não Dobradas/fisiologia
2.
Clin Anat ; 31(6): 891-898, 2018 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-29752839

RESUMO

The mammalian target of rapamycin, mTOR, is a serine-threonine protein kinase downstream of the phosphatidylinositol 3-kinase (PI3K)-AKT axis. The pathway can regulate cell growth, proliferation, and survival by activating ribosomal kinases. Recent studies have implicated the mTOR signaling pathway in ovarian neoplasms, polycystic ovary syndrome (PCOS) and premature ovarian failure (POF). Preclinical investigations have demonstrated that the PI3K/AKT/mTOR pathway is frequently activated in the control of various ovarian functions. mTOR allows cancer cells to escape the normal biochemical system and regulates the balance between apoptosis and survival. Some recent studies have suggested that involvement of the mTOR signaling system is an important pathophysiological basis of PCOS. Overexpression of the mTOR pathway can impair the interaction of cumulus cells, lead to insulin resistance, and affect the growth of follicles directly. The roles of mTOR signaling in follicular development have been extensively studied in recent years; abnormalities in this process lead to a series of pathologies such as POF and infertility. To improve understanding of the role of the mTOR signaling pathway in the pathogenesis and development of ovarian diseases, here we review the roles of mTOR signaling in such diseases and discuss the corresponding therapeutic strategies that target this pathway. Clin. Anat. 31:891-898, 2018. © 2018 Wiley Periodicals, Inc.


Assuntos
Neoplasias Ovarianas/metabolismo , Síndrome do Ovário Policístico/metabolismo , Insuficiência Ovariana Primária/metabolismo , Serina-Treonina Quinases TOR/metabolismo , Feminino , Humanos , Imunossupressores/farmacocinética , Folículo Ovariano/metabolismo , Transdução de Sinais , Sirolimo/farmacocinética , Serina-Treonina Quinases TOR/efeitos dos fármacos
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