Phosphorylation-independent mTORC1 inhibition by the autophagy inducer Rottlerin

Highlights • Rottlerin inhibits proliferation and causes autophagic death in apoptosis-resistant MCF-7 breast cancer cells. • Autophagy is induced by PKCδ-, PP2A, - ERK-, PI3K/AKT-, Bcl2/Beclin- and AMPK-independent mTORC1 inhibition. • Rottlerin inhibits mTORC1 but not mTORC2 activity. • Ex vivo pu...

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Bibliographic Details
Published in:Cancer letters 2015-04, Vol.360 (1), p.17-27
Main Authors: Torricelli, C, Daveri, E, Salvadori, S, Valacchi, G, Ietta, F, Muscettola, M, Carlucci, F, Maioli, E
Format: Article
Language:English
Subjects:
Acetophenones - pharmacology
Adenocarcinoma - enzymology
Adenocarcinoma - genetics
Adenocarcinoma - pathology
AMP-Activated Protein Kinases - metabolism
AMPK
Antibiotics
Antineoplastic Agents - pharmacology
Autophagy
Autophagy - drug effects
Benzopyrans - pharmacology
Breast Neoplasms - enzymology
Breast Neoplasms - genetics
Breast Neoplasms - pathology
Cancer
Experiments
Female
Hematology, Oncology and Palliative Medicine
Humans
Hypoxia
Kinases
MCF-7 Cells
Mechanistic Target of Rapamycin Complex 1
mTOR
Multiprotein Complexes - antagonists & inhibitors
Multiprotein Complexes - metabolism
Phosphatase
Phosphorylation
Polyphenols
Protein Kinase C-delta - metabolism
Protein Kinase Inhibitors - pharmacology
Proteins
Raptor
RNA Interference
Rottlerin
Signal Transduction - drug effects
Time Factors
TOR Serine-Threonine Kinases - antagonists & inhibitors
TOR Serine-Threonine Kinases - genetics
TOR Serine-Threonine Kinases - metabolism
Transfection
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Summary:Highlights • Rottlerin inhibits proliferation and causes autophagic death in apoptosis-resistant MCF-7 breast cancer cells. • Autophagy is induced by PKCδ-, PP2A, - ERK-, PI3K/AKT-, Bcl2/Beclin- and AMPK-independent mTORC1 inhibition. • Rottlerin inhibits mTORC1 but not mTORC2 activity. • Ex vivo pull-down assay demonstrated that Rottlerin directly binds mTOR.
ISSN:0304-3835
1872-7980
DOI:10.1016/j.canlet.2015.01.040