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

. 2022 Feb 4;13(2):118. doi: 10.1038/s41419-022-04576-4

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

© The Author(s) 2022

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 Sorafenib could inhibit Raf/MEK/ERK signaling pathway in all three KIRC cells. After treatment with sorafenib at the same concentration for the same time, the expression of residual phosphorylated ERK was the highest in OS-RC-2 cells. D CCK8 assays of three KIRC cells after sorafenib treatment at the indicated concentrations for 48 h. E Histograms showing the PGK1 protein expression level and IC₅₀ values (48 h) of three KIRC cells. F CCK-8 assay of PGK1-overexpressing and control 786-O cells after sorafenib treatment at the indicated concentrations for 48 h. G PGK1 promoted sorafenib resistance via increasing ERK phosphorylation in 786-O cells. H Schematic diagram of morphological differences between sorafenib-resistant 786-O cells and wild-type 786-O cells. I CCK-8 assay of sorafenib-resistant 786-O cells after sorafenib treatment at the indicated concentrations for 48 h. J Expression levels of PGK1, CXCR4, ERK and its phosphorylation were detected in sorafenib-resistant 786-O cells and wild-type 786-O cells. K Interference with PGK1 expression in our constructed 786-O^-R cells increases their sensitivity to sorafenib. L Schematic diagram of the PGK1-invovled signaling pathway in KIRC progression and sorafenib resistance. In addition to promoting glycolysis to produce ATP for energy supply, PGK1 also induced CXCR4-mediated activation of AKT and ERK phosphorylation to promote tumor growth. Since the RAF/MEK/ERK signaling pathway is one typical target of sorafenib, PGK1 promoted sorafenib resistance via not only accelerating glycolysis but also compensating for the inhibition of ERK phosphorylation caused by sorafenib.