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

. 2018 Apr 11;16:96. doi: 10.1186/s12967-018-1471-1

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

© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

PMC Copyright notice

Fig. 2 — Illustration of MAPK pathway and the role of cisplatin in promoting apoptosis or cell survival. Cisplatin-induced ERK activation phosphorylates p53 which in turn upregulates expression of p21, 45kd-growth arrest and DNA damage (GADD45), and mouse double minute 2 homolog (Mdm2) thereby promoting cell cycle arrest and supporting repair of DNA damage induced by cisplatin. ERK also activates its downstream mediator, RSK which promotes cell survival and metastasis. Cisplatin induced DNA damage activates JNK and p73 and promotes their complex formation and leads to apoptosis. Cisplatin induces stabilization of p18 (Hamlet), a protein regulated by p38 MAPK. This enhances the ability of p53 to interact with and activate pro-apoptotic genes, PUMA and NOXA