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Literature summary for 2.7.11.24 extracted from

  • Ma, B.; Wells, A.
    The mitogen-activated protein (MAP) kinases p38 and extracellular signal-regulated kinase (ERK) are involved in hepatocyte-mediated phenotypic switching in prostate cancer cells (2014), J. Biol. Chem., 289, 11153-11161.
    View publication on PubMedView publication on EuropePMC
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Activating Compound

Activating Compound Comment Organism Structure
additional information ERK1/2 are phosphorylated and activated by MAPK kinases MEK1/MEK2 Homo sapiens
additional information p38 is phosphorylated and activated by MAPK kinases MEK Homo sapiens

Organism

Organism UniProt Comment Textmining
Homo sapiens
-
-
-

Posttranslational Modification

Posttranslational Modification Comment Organism
phosphoprotein ERK1/2 are phosphorylated and activated by MAPK kinases MEK1/MEK2 Homo sapiens
phosphoprotein p38 is phosphorylated and activated by MAPK kinases MEK6 Homo sapiens

Source Tissue

Source Tissue Comment Organism Textmining
A-549 cell
-
 Homo sapiens
-
DU-145 cell
-
 Homo sapiens
-
hepatocyte
-
 Homo sapiens
-
PCa cell
-
 Homo sapiens
-
prostate cancer cell
-
 Homo sapiens
-

Synonyms

Synonyms Comment Organism
ERK
-
 Homo sapiens
ERK1/2
-
 Homo sapiens
MAPK
-
 Homo sapiens
p38
-
 Homo sapiens
p38alpha
-
 Homo sapiens

General Information

General Information Comment Organism
malfunction inhibition of ERK MAPK activity increased E-cadherin expression at both the transcriptional and protein level. Knockdown of EKR1/2 expression by siRNA in A-549 cells produces a similar up-regulation of E-cadherin. Inhibition of p38 and ERK1/2 activities but not JNK and PI3K abrogates DU145 cells survival advantage Homo sapiens
malfunction inhibition of p38 MAPK activity increased E-cadherin expression at both the transcriptional and protein level. Knockdown of p38alpha expression by siRNA in A-549 cells produces a similar upregulation of E-cadherin. Inhibition of p38 and ERK1/2 activities but not JNK and PI3K abrogates DU145 cells survival advantage Homo sapiens
metabolism hepatocyte coculture induces the re-expression of E-cadherin via abrogation of autocrine EGFR signaling pathway in prostate cancer (PCa) cells and this confers a survival advantage. Hepatocytes educate PCa cells to undergo mesenchymal to epithelial reverting transition (MErT) by modulating the activity of p38 and ERK1/2. Hepatocytes inhibit p38 and ERK1/2 activity in prostate cancer cells, which allows E-cadherin re-expression. Introduction of constitutively active MEK6 and MEK1 to DU-145 cells cocultured with hepatocytes abrogates E-cadherin re-expression. At least a partial phenotypic reversion can be achieved by suppression of p38 and ERK1/2 activation in DU-145 cells even in the absence of hepatocytes Homo sapiens