Autophagic flux blockage by accumulation of weakly basic tenovins leads to elimination of B-Raf mutant tumour cells that survive vemurafenib

• Main Authors: Ladds M.J.G.W., Pastor-Fernández A., Popova G., van Leeuwen I.M.M., Eng K.E., Drummond C.J., Johansson L., Svensson R., Westwood N.J., McCarthy A.R., Tholander F., Popa M., Lane D.P., McCormack E., McInerney G.M., Bhatia R., Laín S.
• Other Authors: MEDICINE
• Format: Article
• Published: 2019
• Subjects: antineoplastic agent; B Raf kinase; chloroquine; protein p53; sirtuin 1; tenovin; tenovin 1; tenovin 33; tenovin 39; tenovin 39 oh; tenovin 50; tenovin 50 oh; tenovin 6; tenovin D1; tenovin D3; tertiary amine; unclassified drug; vemurafenib; benzamide derivative; BRAF protein, human; indole derivative; sirtuin; sulfonamide; tenovin-6; TP53 protein, human; Article; autophagy; cell death; cell survival; drug mechanism; G1 phase cell cycle checkpoint; human; human cell; melanoma cell; cell proliferation; chemical structure; chemistry; drug effect; drug potentiation; drug resistance; gene expression regulation; genetics; melanoma; mutation; tumor cell line; Antineoplastic Agents; Autophagy; Benzamides; Cell Line, Tumor; Cell Proliferation; Cell Survival; Drug Resistance, Neoplasm; Drug Synergism; Gene Expression Regulation, Neoplastic; Humans; Indoles; Melanoma; Molecular Structure; Mutation; Proto-Oncogene Proteins B-raf; Sirtuins; Sulfonamides; Tumor Suppressor Protein p53
• Online Access: https://scholarbank.nus.edu.sg/handle/10635/161233
• Institution: National University of Singapore

10.1371/journal.pone.0195956