Contents
20 August 2019
Vol 12, Issue 595
Vol 12, Issue 595
Focus
- Dynamics of drug response informs rational combination regimens
Metabolic reprogramming could be targeted to eliminate drug-tolerant cancer cells (Goldman et al., in 20 August 2019 issue).
Research Articles
- Targeting tumor phenotypic plasticity and metabolic remodeling in adaptive cross-drug tolerance
Resistance to unrelated chemotherapeutics in breast cancer cells is caused by a metabolic switch.
- Reverse signaling by semaphorin 4C elicits SMAD1/5- and ID1/3-dependent invasive reprogramming in cancer cells
As a receptor, semaphorin 4C hijacks TGF-β signaling to promote metastatic breast cancer growth.
Editors' Choice
- Parkin protects against necroptosis
Activation of Parkin by AMPK-mediated phosphorylation inhibits RIPK3 and prevents necroptosis.
About The Cover
Online Cover This week features a Research Article that describes how a metabolic switch in taxane-treated breast cancer cells results in increased reliance on oxidative and non-oxidative glucose metabolism and in resistance to unrelated chemotherapeutics (also see the associated Focus). The image shows immunohistochemistry of breast tumors from taxane-treated mice for the glucose transporter Glut1 (red) and CD44 (green), a marker for the metabolic switch. [Image: Goldman et al./Science Signaling]
