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Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation. | LitMetric

AI Article Synopsis

  • - ALCL is a rare and aggressive type of non-Hodgkin's lymphoma that typically affects younger individuals, with a significant portion exhibiting a specific genetic translocation associated with a fusion protein (NPM-ALK) that makes treatment different from ALK-negative forms.
  • - High levels of miR-155 are found in ALCL ALK(-) cases, which correlate with worse outcomes; this microRNA negatively regulates key proteins involved in tumor suppression, such as C/EBPβ and SOCS1.
  • - Targeting miR-155 in ALCL ALK(-) models shows promise for reducing tumor growth and altering cancer-related signaling pathways, indicating that inhibiting miR-155 could be a potential therapeutic

Article Abstract

Anaplastic large cell lymphoma (ALCL) is a rare, aggressive, non-Hodgkin's lymphoma that is characterized by CD30 expression and disease onset in young patients. About half of ALCL patients bear the t(2;5)(p23;q35) translocation, which results in the formation of the nucleophosmin-anaplastic lymphoma tyrosine kinase (NPM-ALK) fusion protein (ALCL ALK(+)). However, little is known about the molecular features and tumour drivers in ALK-negative ALCL (ALCL ALK(-)), which is characterized by a worse prognosis. We found that ALCL ALK(-), in contrast to ALCL ALK(+), lymphomas display high miR-155 expression. Consistent with this, we observed an inverse correlation between miR-155 promoter methylation and miR-155 expression in ALCL. However, no direct effect of the ALK kinase on miR-155 levels was observed. Ago2 immunoprecipitation revealed miR-155 as the most abundant miRNA, and enrichment of target mRNAs C/EBPβ and SOCS1. To investigate its function, we over-expressed miR-155 in ALCL ALK(+) cell lines and demonstrated reduced levels of C/EBPβ and SOCS1. In murine engraftment models of ALCL ALK(-), we showed that anti-miR-155 mimics are able to reduce tumour growth. This goes hand-in-hand with increased levels of cleaved caspase-3 and high SOCS1 in these tumours, which leads to suppression of STAT3 signalling. Moreover, miR-155 induces IL-22 expression and suppresses the C/EBPβ target IL-8. These data suggest that miR-155 can act as a tumour driver in ALCL ALK(-) and blocking miR-155 could be therapeutically relevant. Original miRNA array data are to be found in the supplementary material (Table S1).

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4557053PMC
http://dx.doi.org/10.1002/path.4539DOI Listing

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