Summary
Published in Biochemical and Biophysical Research Communications (2016), this peer-reviewed study used 3D Petri Dish® micro-molds to form scaffold-free 3D microtissues. Full citation: Ushijima, Hironori, et al. Anisomycin-induced GATA-6 degradation accompanying a decrease of proliferation of colorectal cancer cell
Anisomycin-induced GATA-6 degradation accompanying a decrease of proliferation of colorectal cancer cell
Research Overview
The transcription factor GATA-6 guides normal mesoderm and endoderm differentiation but is abnormally overexpressed in many gastrointestinal cancers, where it accelerates proliferation and anti-apoptotic responses. The authors had previously shown that JNK signaling causes GATA-6 proteolysis.
Here they demonstrated that anisomycin, a JNK activator, stimulates nuclear export of GATA-6 in the colorectal cancer line DLD-1 and markedly inhibits proliferation via G2/M arrest in plate culture — though without inducing apoptosis under those conditions, making the 3D comparison informative.
Key Discoveries
- Anisomycin stimulated nuclear export of GATA-6 in colorectal cancer cells
- Proliferation inhibited via G2/M arrest without apoptosis induction in plate culture
- Links JNK activation to degradation of a transcription factor overexpressed in GI cancers
