Wnt3a Treatment Induces Transcriptional Upregulation of CTGF in HEK-293A and MCF7 Cells
Loading...
Authors
Park, Sung Soo
Issue Date
2019
Type
Thesis
Language
en_US
Keywords
Alternative Title
Abstract
The Wnt signaling pathway and the Hippo signaling pathway play critical roles in cell fate determination and proliferation. Despite the fact that two pathways were initially established as separate and independent cascades, recent studies have found evidence for possible cross-talk between the Wnt and the Hippo signaling pathways. It has been revealed that few target genes of the Wnt pathway, such as CD44, stimulates the activity of the Hippo pathway by interacting with its core component NF2, and that the molecules involved in Wnt pathway, such as TCF and β-catenin, upregulate the Hippo pathway in a similar manner. To confirm the largely speculated existence of the cross-talk between the two pathways in human cells, we treated HEK-293A and MCF-7 cells with Wnt3a ligand. We investigated the changes in transcription levels of CTGF and Axin-2 and changes in the intracellular quantity of β-catenin and phosphorylated YAP. We observed that CTGF and Axin-2 transcription was stimulated, the β-catenin level was increased, and phosphorylated YAP level was decreased upon Wnt3a treatment. Taken together, our results offer evidence for the crosstalk between the Wnt and the Hippo signaling pathways in human cells. Future studies should investigate other candidate molecules of the Wnt pathway that may interact with the Hippo pathway, as well as identify their downstream effects in regards to embryogenesis and cell fate determination. The effect of Hippo pathway activation on the Wnt pathway should be investigated as well to shed light on the intricate reciprocal regulation process between the two signaling pathways.
Description
iv, 24 p.
Citation
Publisher
Kalamazoo College
License
U.S. copyright laws protect this material. Commercial use or distribution of this material is not permitted without prior written permission of the copyright holder.