Targeting the glucose-regulated protein-78 abrogates Pten-null driven AKT activation and endometrioid tumorigenesis

Rates of the most common gynecologic cancer, endometrioid adenocarcinoma (EAC), continue to rise, mirroring the global epidemic of obesity, a well-known EAC risk factor. Thus, identifying novel molecular targets to prevent and/or mitigate EAC is imperative. The prevalent Type 1 EAC commonly harbors...

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Veröffentlicht in:	Oncogene 2015-10, Vol.34 (43), p.5418-5426
Hauptverfasser:	Lin, Y G, Shen, J, Yoo, E, Liu, R, Yen, H-Y, Mehta, A, Rajaei, A, Yang, W, Mhawech-Fauceglia, P, DeMayo, F J, Lydon, J, Gill, P, Lee, A S
Format:	Artikel
Sprache:	eng
Schlagworte:	1-Phosphatidylinositol 3-kinase 14 14/19 45/77 631/67/1517/1931 64/60 82/1 82/80 96/2 Adenocarcinoma AKT protein Animals Antibodies, Monoclonal - pharmacology Apoptosis Apoptosis - drug effects Binding proteins Carcinogenesis - drug effects Carcinogenesis - metabolism Carcinoma, Endometrioid - drug therapy Carcinoma, Endometrioid - metabolism Cell Biology Cell surface Clonal deletion Development and progression Endometrial cancer Endometrium Endoplasmic reticulum Endoplasmic Reticulum - drug effects Endoplasmic Reticulum - metabolism Epithelium Female Glucose Gynecology Heat-Shock Proteins - metabolism Homeostasis Human Genetics Hyperplasia Internal Medicine Male Medicine Medicine & Public Health Mice Mice, Inbred C57BL Mice, Knockout Molecular Chaperones - metabolism Monoclonal antibodies Oncology original-article Phosphatidylinositol 3-Kinase - metabolism Physiological aspects Progesterone Protein kinases Proteins Proto-Oncogene Proteins c-akt - metabolism PTEN Phosphohydrolase - metabolism PTEN protein Recombinase Risk factors Signal Transduction - drug effects Therapeutic targets Tumor suppressor genes Tumorigenesis
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