ArticleCell death & disease2018
FBXL10 contributes to the development of diffuse large B-cell lymphoma by epigenetically enhancing ERK1/2 signaling pathway.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Multiomics reveals glutathione metabolism as a driver of bimodality during stem cell aging.Cell metabolism · 2023Article
- Article
- KDM2B Overexpression Facilitates LyticJournal of virology · 2021Article
- Deregulation of tumor suppressive ASXL1-PTEN/AKT axis in myeloid malignancies.Journal of molecular cell biology · 2020Article
- FBN1 promotes DLBCL cell migration by activating the Wnt/β-catenin signaling pathway and regulating TIMP1.American journal of translational research · 2020Article
- FBXL10 regulates cardiac dysfunction in diabetic cardiomyopathy via the PKC β2 pathway.Journal of cellular and molecular medicine · 2019Article
- Epigenetic Targets in Synovial Sarcoma: A Mini-Review.Frontiers in oncology · 2019Review
- KDM2B regulates choline kinase expression and neuronal differentiation of neuroblastoma cells.PloS one · 2019Article
- Epstein-Barr Virus Nuclear Antigen 3C Inhibits Expression ofJournal of virology · 2018Article
- PRMT2 links histone H3R8 asymmetric dimethylation to oncogenic activation and tumorigenesis of glioblastoma.Nature communications · 2018Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epigenetic modifiers have emerged as critical factors governing the biology of different cancers. Herein we show that FBXL10 (also called KDM2B or JHDM1B), an important member of Polycomb repressive complexes, is overexpressed in human diffuse large B-cell lymphoma (DLBCL) tissues and the derived cell lines. Knocking down FBXL10 by specific short hairpin RNAs in DLBCL cells inhibits cell proliferation and induces apoptosis in vitro. Moreover, FBXL10 depletion in DLBCL cells abrogates tumor growth in mouse xenograft models. Through the analysis of RNA sequencing, we find that one of the key derepressed genes by depletion of FBXL10 is DUSP6, encoding a phosphatase for ERK1/2. Mechanistically FBXL10 maintains the silencing of DUSP6 expression via recruitment of Polycomb group proteins and deposition of repressive histone modifications at the DUSP6 promoter. Consistently, FBXL10 is required for ERK1/2 phosphorylation in DLBCL cells. Furthermore, we show that ERK1/2 activation and the proliferation rate of FBXL10-depleted cells can be rescued by downregulation of DUSP6 expression. These findings indicate that FBXL10 may be a promising therapeutic target in DLBCL and establish a link of epigenetic regulators to kinase signaling pathways.
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