ReferenceID 3729

Phosphorylation-independent mTORC1 inhibition by the autophagy inducer Rottlerin

Cancer Lett

We recently found that Rottlerin not only inhibits proliferation but also causes Bcl-2- and Beclin 1-independent autophagic death in apoptosis-resistant breast adenocarcinoma MCF-7 cells. Having excluded a role for cano

Back to Browse

Relationship Network

Interactive first-hop connections across herbs, ingredients, formulas, targets, diseases, symptoms, syndromes, evidence, and monographs.

Click a node to open it in a new tab
Ingredient: 1Reference: 1Links: 1
Arranging relationship network...

Record Fields

Scalar fields from the final reference record.

Reference Id
3729
Evidence Id
20319
Core Evidence Id
20319
Source Reference Id
736
Herb2 Reference Id
HBREF001269
Subject Paper Key
HBIN042467_25661734
Pubmed Id
25661734
Doi
10.1016/j.canlet.2015.01.040
Paper Title
Phosphorylation-independent mTORC1 inhibition by the autophagy inducer Rottlerin
Paper Abstract
We recently found that Rottlerin not only inhibits proliferation but also causes Bcl-2- and Beclin 1-independent autophagic death in apoptosis-resistant breast adenocarcinoma MCF-7 cells. Having excluded a role for canonical signaling pathways, the current study was aimed to investigate the contribution of the AMPK/mTOR axis in autophagy induction and to search for the upstream signaling molecules potentially targeted by Rottlerin. Using several enzyme inhibitors, Western blotting analysis, mTOR siRNA and pull down assay, we demonstrate that the Rottlerin-triggered autophagy is mediated by inhibition of mTORC1 activity through a novel AMPK and mTORC1 phosphorylation-independent mechanism, likely mediated by the direct interaction between Rottlerin and mTOR.
Journal
Cancer Lett
Publish Year
2015
Experiment Subject
apoptosis-resistant breast adenocarcinoma mcf-7 cells
Experiment Type
Cell Experiment
Phenotype Related
Paper Title Cn
Paper Title En
Phosphorylation-independent mTORC1 inhibition by the autophagy inducer Rottlerin
Bilingual Status
semi_complete