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

. 2020 Apr 29;9(4):42. doi: 10.1038/s41389-020-0226-z

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

© The Author(s) 2020

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 8 — a c-Myc expression was higher in patients with higher ACSL4 expression, as suggested by IHC staining (scale bar: 20 μm; magnification: ×400). b Correlation between ACSL4 levels and nuclear expression of c-Myc in an HCC array. The histogram (right) showed the percentages of tumors with low or high nuclear expression of c-Myc in those with low (n = 25) or high (n = 18) expression of ACSL4. ***p < 0.001. The correlations were assessed with χ² test. c Our results suggest a model in which depletion of ACSL4 results in reduction of p-ERK, thus decreases phospho-S62 c-Myc and increases the expression of one of the c-Myc E3 ubiquitin ligases, FBW7. Dephosphorylation c-Myc at S62 in the context of phospho-T58 and FBW7 overexpression thereby results in the ubiquitin-mediated degradation of c-Myc. As such, ACSL4 depletion ultimately results in the inhibition of c-Myc oncogenic activity and suppressed hepatocellular carcinogenesis.