ArticleThe Journal of biological chemistry2014
The mitogen-activated protein (MAP) kinases p38 and extracellular signal-regulated kinase (ERK) are involved in hepatocyte-mediated phenotypic switching in prostate cancer cells.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- From biology to the clinic - exploring liver metastasis in prostate cancer.Nature reviews. Urology · 2024Review
- Prostate cancer cells synergistically defend against CD8Cancer medicine · 2023Article
- Resistance to tyrosine kinase inhibitors promotes renal cancer progression through MCPIP1 tumor-suppressor downregulation and c-Met activation.Cell death & disease · 2022Article
- Interferon-γ increases sensitivity to chemotherapy and provides immunotherapy targets in models of metastatic castration-resistant prostate cancer.Scientific reports · 2022Article
- Thorny ground, rocky soil: Tissue-specific mechanisms of tumor dormancy and relapse.Seminars in cancer biology · 2022Review
- The Molecular Mechanism of Aerobic Exercise Improving Vascular Remodeling in Hypertension.Frontiers in physiology · 2022Review
- Autophagy and Hepatic Tumor Microenvironment Associated Dormancy.Journal of gastrointestinal cancer · 2021Review
- The liver metastatic niche: modelling the extracellular matrix in metastasis.Disease models & mechanisms · 2021Review
- A Perspective on Therapeutic Pan-Resistance in Metastatic Cancer.International journal of molecular sciences · 2020Review
- Downregulation of uPAR promotes urokinase translocation into the nucleus and epithelial to mesenchymal transition in neuroblastoma.Journal of cellular physiology · 2020Article
- The pan-therapeutic resistance of disseminated tumor cells: Role of phenotypic plasticity and the metastatic microenvironment.Seminars in cancer biology · 2020Review
- Article
- Total Panax notoginseng saponin inhibits balloon injury-induced neointimal hyperplasia in rat carotid artery models by suppressing pERK/p38 MAPK pathways.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2020Article
- miR-137-3p Modulates the Progression of Prostate Cancer by Regulating the JNK3/EZH2 Axis.OncoTargets and therapy · 2020Article
- Expression of E-cadherin and specific CXCR3 isoforms impact each other in prostate cancer.Cell communication and signaling : CCS · 2019Article
- Role of the Balance of Akt and MAPK Pathways in the Exercise-Regulated Phenotype Switching in Spontaneously Hypertensive Rats.International journal of molecular sciences · 2019Article
- The molecular biology of prostate cancer: current understanding and clinical implications.Prostate cancer and prostatic diseases · 2018Review
- Inhibition of FOXC2 restores epithelial phenotype and drug sensitivity in prostate cancer cells with stem-cell properties.Oncogene · 2016Article
- Liver protects metastatic prostate cancer from induced death by activating E-cadherin signaling.Hepatology (Baltimore, Md.) · 2016Article
- Macrophage phenotypic subtypes diametrically regulate epithelial-mesenchymal plasticity in breast cancer cells.BMC cancer · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The greatest challenge for the seeding of cancer in metastatic sites is integration into the ectopic microenvironment despite the lack of an orthotopic supportive environment and presence of pro-death signals concomitant with a localized "foreign-body" inflammatory response. In this metastatic location, many carcinoma cells display a reversion of the epithelial-to-mesenchymal transition that marks dissemination in the primary tumor mass. This mesenchymal to epithelial reverting transition (MErT) is thought to help seeding and colonization by protecting against cell death. We have previously shown that hepatocyte coculture induces the re-expression of E-cadherin via abrogation of autocrine EGFR signaling pathway in prostate cancer (PCa) cells and that this confers a survival advantage. Herein, we show that hepatocytes educate PCa to undergo MErT by modulating the activity of p38 and ERK1/2. Hepatocytes inhibited p38 and ERK1/2 activity in prostate cancer cells, which allowed E-cadherin re-expression. Introduction of constitutively active MEK6 and MEK1 to DU145 cells cocultured with hepatocytes abrogated E-cadherin re-expression. At least a partial phenotypic reversion can be achieved by suppression of p38 and ERK1/2 activation in DU145 cells even in the absence of hepatocytes. Interestingly, these mitogen-activated protein kinase activities were also triggered by re-expressed E-cadherin leading to p38 and ERK1/2 activity in PCa cells; these signals provide protection to PCa cells upon challenge with chemotherapy and cell death-inducing cytokines. We propose that distinct p38/ERK pathways are related to E-cadherin levels and function downstream of E-cadherin allowing, respectively, for hepatocyte-mediated MErT and tumor cell survival in the face of death signals.
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