PUBLICATION

The MRPS18-2 protein levels correlate with prostate tumor progression and it induces CXCR4-dependent migration of cancer cells

Authors
Mushtaq, M., Jensen, L., Davidsson, S., Grygoruk, O.V., Andrén, O., Kashuba, V., Kashuba, E.
ID
ZDB-PUB-180206-5
Date
2018
Source
Scientific Reports   8: 2268 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Antigens, CD/metabolism*
  • Cadherins/metabolism*
  • Cell Movement*
  • Cytological Techniques
  • Disease Models, Animal
  • Disease Progression
  • Epithelial-Mesenchymal Transition
  • Histocytochemistry
  • Humans
  • Immunohistochemistry
  • Male
  • Prostatic Neoplasms/pathology*
  • Receptors, CXCR4/metabolism*
  • Repressor Proteins/analysis*
  • Ribosomal Proteins/analysis*
  • Tumor Cells, Cultured
  • Twist-Related Protein 1/analysis*
  • Zebrafish
PubMed
29396484 Full text @ Sci. Rep.
Abstract
We have earlier found abnormal expression of the mitochondrial ribosomal protein S18-2 (MRPS18-2, S18-2) in endometrial cancer, compared to the expression in hyperplasia and in normal endometrium. Here we report that expression of S18-2 was increased with disease progression in clinical specimens of prostate cancer (PCa). The level of induction of epithelial to mesenchymal cell transition (EMT) correlated with the expression level of S18-2 in PCa cell lines. Moreover, cells acquired increased ability of migration upon S18-2 overexpression, as was evaluated in zebrafish embryo model and in trans-well assay. We found that this is due to increased CXCR4 cell surface expression. Neutralizing CXCR4 protein or abrogating S18-2 expression in cells significantly reduced their migratory ability directed toward CXCL12. The mRNA expression of TWIST2, encoding one of transcription factors that induce EMT upon CXCR4 increase, positively correlated with the S18-2 protein level. Together, these data suggest that the S18-2 protein induces EMT through the TWIST2/E-cadherin signalling and, consequently, CXCR4-mediated migration of PCa cells.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping