Flcn-deficient renal cells are tumorigenic and sensitive to mTOR suppression

• Main Authors: Wu, M, Si, S, Li, Y, Schoen, S, Xiao, G.-Q, Li, X, Teh, B.T, Wu, G, Chen, J
• Other Authors: DUKE-NUS MEDICAL SCHOOL
• Format: Article
• Published: 2020
• Subjects: estrone; mammalian target of rapamycin; rapamycin; antineoplastic agent; Bhd protein, mouse; FLCN protein, human; MTOR protein, human; mTOR protein, mouse; oncoprotein; protein kinase inhibitor; target of rapamycin kinase; tumor suppressor protein; animal cell; animal experiment; animal model; animal tissue; antineoplastic activity; Article; Birt Hogg Dube syndrome; cancer inhibition; carcinogenesis; controlled study; human; human cell; kidney carcinoma; kidney tubule cell; mouse; nonhuman; phenotype; signal transduction; tumor xenograft; upregulation; allograft; animal; antagonists and inhibitors; Carcinoma, Renal Cell; cell transformation; deficiency; drug effects; drug screening; enzymology; gene expression regulation; genetic predisposition; genetics; Kidney Neoplasms; knockout mouse; metabolism; molecularly targeted therapy; nude mouse; pathology; time factor; tumor cell line; tumor volume; Allografts; Animals; Antineoplastic Agents; Cell Line, Tumor; Cell Transformation, Neoplastic; Gene Expression Regulation, Neoplastic; Genetic Predisposition to Disease; Humans; Mice, Knockout; Mice, Nude; Molecular Targeted Therapy; Phenotype; Protein Kinase Inhibitors; Proto-Oncogene Proteins; Signal Transduction; Sirolimus; Time Factors; TOR Serine-Threonine Kinases; Tumor Burden; Tumor Suppressor Proteins; Xenograft Model Antitumor Assays
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/180935
• Institution: National University of Singapore

10.18632/oncotarget.5018