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

. 2021 May 31;11:11376. doi: 10.1038/s41598-021-89765-5

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

© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Graphical illustration of high glucose induced EMT via c-Met activation, its downstream signaling and associated biological cellular responses in high glucose and c-Met inhibited conditions. Green and red colored mechanisms represent active and inhibited c-Met signaling conditions, respectively. Molecular mechanisms defined in this study are summarized and numbered as following: (1) High glucose induces ligand-independent homodimerization of c-Met which in turn (2) activation of c-Met and downstream signaling, (3) promotes mesenchymal phenotype via inducing Vimentin (VIM) and N-Cadherin (CDH2) expression, (4) induces motility, invasion and spheroid formation ability. (5) Inhibition of c-Met activity by a small molecule inhibitor (SU11274) alters expression of glucose metabolism genes, (6) reverses high glucose induced mesenchymal-like phenotype and (7) aggressive behavior and eventually sensitizes HCC cells to glucose toxicity and promotes apoptosis. c-Met activated (A) and inhibited (B) conditions. Glucose metabolism genes which are confirmed with only one cell line are typed in with standard fonts, two cell lines are typed in with “bold” fonts and the genes confirmed in both in-vitro and bioinformatic analyses are typed with “big bold” fonts. Created with BioRender.com.