ArticleThe Journal of pathology2015
Oncogenic role of miR-155 in anaplastic large cell lymphoma lacking the t(2;5) translocation.
Article in The Journal of pathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Beyond the Surface: Deciphering the Role of Genetic Susceptibility in BIA-ALCL Pathogenesis.Biomedicines · 2026Review
- The role of IL-22 in cancer.Medical oncology (Northwood, London, England) · 2024Review
- Th17 cell-derived miR-155-5p modulates interleukin-17 and suppressor of cytokines signaling 1 expression during the progression of systemic sclerosis.Journal of clinical laboratory analysis · 2022Article
- New Advances in Liquid Biopsy Technologies for Anaplastic Lymphoma Kinase (ALK)-Positive Cancer.Cancers · 2021Review
- The Role of microRNA in Pathogenesis, Diagnosis, Different Variants, Treatment and Prognosis of Mycosis Fungoides.Frontiers in oncology · 2021Review
- Impact ofFrontiers in oncology · 2021Article
- Article
- Epigenetic alterations and advancement of treatment in peripheral T-cell lymphoma.Clinical epigenetics · 2020Review
- Review
- Epigenetic aberrations in natural killer/T-cell lymphoma: diagnostic, prognostic and therapeutic implications.Therapeutic advances in medical oncology · 2020Review
- MiR-155 promotes anaplastic thyroid cancer progression by directly targeting SOCS1.BMC cancer · 2019Article
- STAT3 Dysregulation in Mature T and NK Cell Lymphomas.Cancers · 2019Review
- STAT3 and STAT5 Activation in Solid Cancers.Cancers · 2019Review
- Review
- MicroRNA-155: A Master Regulator of Inflammation.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2019Review
- Article
- Oncogenic activation of the STAT3 pathway drives PD-L1 expression in natural killer/T-cell lymphoma.Blood · 2018Article
- MiRNA Dysregulation in Childhood Hematological Cancer.International journal of molecular sciences · 2018Review
- Crosstalk between microRNA and DNA Methylation Offers Potential Biomarkers and Targeted Therapies in ALK-Positive Lymphomas.Cancers · 2017Review
- The heterogeneous landscape of ALK negative ALCL.Oncotarget · 2017Review
Corrections and comments
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Authors and funding
18 authors at 8 institutions in 3 countries.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.