Journal
PLOS ONE
Volume 10, Issue 4, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0122517
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Funding
- Fonds National de la Recherche Scientifique (FNRS) (Belgium)
- Centre du Cancer (Cliniques Universitaires Saint-Luc, UCL, Belgium)
- Fondation Contre le Cancer (Belgium)
- FNRS (FRSM) [3.4.559.08.F]
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Loss of expression of surface antigens represents a significant problem for cancer immunotherapy. Microphthalmia-associated transcription factor (MITF-M) regulates melanocyte fate by driving expression of many differentiation genes, whose protein products can be recognized by cytolytic T lymphocytes. We previously reported that interleukin-1 beta (IL-1 beta) can downregulate MITF-M levels. Here we show that downregulation of MITF-M expression by IL-1 beta was paralleled by an upregulation of miR-155 expression in four melanoma lines. We confirmed that miR-155 was able to target endogenous MITF-M in melanoma cells and demonstrated a role for miR-155 in the IL-1 beta-induced repression of MITF-M by using an antagomiR. Notably, we also observed a strong negative correlation between MITF-M and miR-155 levels in a mouse model of melanoma. Taken together, our results indicate that MITF-M downregulation by inflammatory stimuli might be partly due to miR-155 upregulation. This could represent a novel mechanism of melanoma immune escape in an inflammatory microenvironment.
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