Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2018 Nov 30;10(12):476. doi: 10.3390/cancers10120476

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Propranolol synergizes with the glycolytic inhibitor dichloroacetate (DCA) to dramatically attenuate tumor cell metabolism and mTOR signaling. Metabolic profile schematic (A), representing possible shifts in metabolic phenotype compared to control. Metabolic profiles of mEERL (B) and MLM3 cells (C) treated overnight with propranolol (40 µM) and/or DCA (10 mM). Values reflect the average of n = 3–5 independent biological replicates +/− SEM. Values were adjusted for non-glycolytic acidification and normalized to total protein. Western blot (D) assessing mTOR activity via p70S6K phosphorylation in mEERL (left) and MLM3 cells (right) following overnight treatment with propranolol (40 µM) and/or DCA (10 mM). Spot densitometry was used to calculate fold change in phosphorylated/total p70S6K signal intensity relative to control for each cell line.