Logo image
Activation of p38α stress-activated protein kinase drives the formation of the pre-metastatic niche in the lungs
Journal article   Peer reviewed

Activation of p38α stress-activated protein kinase drives the formation of the pre-metastatic niche in the lungs

Jun Gui, Farima Zahedi, Angelica Ortiz, Christina Cho, Kanstantsin V Katlinski, Kevin Alicea-Torres, Jinyang Li, Leslie Todd, Hongru Zhang, Daniel P Beiting, …
Nature cancer, Vol.1(6), pp.603-619
06/01/2020
DOI: 10.1038/s43018-020-0064-0
PMCID: PMC8194112
PMID: 34124690
url
https://www.ncbi.nlm.nih.gov/pmc/articles/8194112View
Open Access

Abstract

Primary tumor-derived factors (TDFs) act upon normal cells to generate a pre-metastatic niche, which promotes colonization of target organs by disseminated malignant cells. Here we report that TDFs-induced activation of the p38α kinase in lung fibroblasts plays a critical role in the formation of a pre-metastatic niche in the lungs and subsequent pulmonary metastases. Activation of p38α led to inactivation of type I interferon signaling and stimulation of expression of fibroblast activation protein (FAP). FAP played a key role in remodeling of the extracellular matrix as well as inducing the expression of chemokines that enable lung infiltration by neutrophils. Increased activity of p38 in normal cells was associated with metastatic disease and poor prognosis in human melanoma patients whereas inactivation of p38 suppressed lung metastases. We discuss the p38α-driven mechanisms stimulating the metastatic processes and potential use of p38 inhibitors in adjuvant therapy of metastatic cancers.
Fibroblasts - pathology Humans Lung - pathology Lung Neoplasms - pathology Protein Kinases Signal Transduction

Details

Metrics

3 Record Views
Logo image