Nuclear Translocation of Met Via Internet Mechanism

<p>MET is one of the receptor tyrosine kinases (RTKs) that are overexpressed in malignant cancer types, including breast cancer. While RTKs are traditionally known for their roles in signaling transduction from the cell surface, recent studies have provided evidence demonstrating that most of RTKs can translocate into nucleus to regulate cellular processes in response to both ligand and stress stimulation. Oxidative stress is a common stress in cancer cells due to alteration of metabolism, and constitutive oxidative stress related to reactive oxygen species (ROS) has been observed in breast cancer cells. Here, we show that hepatocyte growth factor (HGF) as well as hydrogen peroxide (H₂O₂) can induce nuclear translocation of full-length MET holoreceptor via a membrane-bound vesicle transport mechanism in breast cancer cells. Our findings provide a putative mechanism by which breast cancer cells adapt to oxidative stress.</p>

Name thesis:degree_name

Masters of Science (MS)

Level thesis:degree_level

Thesis (MS)

Year dc:date.available

2014

Author dc:creator

• CHEN, MEI-KUANG

Contributors dc:contributor

• Mien-Chie Hung Ph.D.
• Paul J. Chiao Ph.D.
• Min Gyu Lee Ph.D.

• MET
• oncogene
• nuclear transport
• breast cancer
• hepatocyte growth factor receptor
• ROS
• Cancer Biology

Repository record dc:identifier

https://digitalcommons.library.tmc.edu/utgsbs_dissertations/504

OAI identifier oai:identifier

oai:digitalcommons.library.tmc.edu:utgsbs_dissertations-1543