ArticleCancer biology & medicine2019
Targeting EZH1/2 induces cell cycle arrest and inhibits cell proliferation through reactivation of p57
Article in Cancer biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
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- Xist RNA dependent and independent mechanisms regulate dynamic X chromosome inactivation in B lymphocytes.Cell reports · 2026Article
- Targeting signaling pathways in lymphoma: From molecular mechanisms to clinical breakthroughs.Chinese medical journal · 2026Review
- EZH2 suppresses the chemosensitivity of diffuse large B cell lymphoma via regulating TP53INP1.Clinical and experimental medicine · 2025Article
- Pharmacological Advancements of PRC2 in Cancer Therapy: A Narrative Review.Life (Basel, Switzerland) · 2024Review
- Bioinformatics study of bortezomib resistance-related proteins and signaling pathways in mantle cell lymphoma.Translational cancer research · 2024Article
- Causal Effects of Oxidative Stress on Diabetes Mellitus and Microvascular Complications: Insights Integrating Genome-Wide Mendelian Randomization, DNA Methylation, and Proteome.Antioxidants (Basel, Switzerland) · 2024Article
- Lappaol F regulates the cell cycle by activating CDKN1C/p57 in human colorectal cancer cells.Pharmaceutical biology · 2023Article
- Triple targeting of RSK, AKT, and S6K as pivotal downstream effectors of PDPK1 by TAS0612 in B-cell lymphomas.Cancer science · 2023Article
- Article
- Targeting Protein Degradation Pathways in Tumors: Focusing on their Role in Hematological Malignancies.Cancers · 2022Review
- Article
- CircCDYL Serves as a New Biomarker in Mantle Cell Lymphoma and Promotes Cell Proliferation.Cancer management and research · 2019Article
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the effect of dysregulation of epigenetic regulator EZH1 and EZH2 on the proliferation in MCL and the underlying mechanisms.
methodsIn this study, we elucidated the role of EZH1 and EZH2 overexpression by immunohistochemistry and correlated them to clinical outcome in 41 MCL patients. Quantitative real-time PCR and Western blot were applied to confirm the level of EZH1 and EZH2 in well-characterized MCL cell lines which were compared to those of naïve B cells. Then we manipulated the expression of EZH1 and EZH2 in MCL cells using CRISPR/Cas9 system to directly investigate their functional roles in MCL. We also evaluated the effect of two small molecule selective inhibitors, EPZ005687 and UNC1999, on MCL cell proliferation, cell cycle distribution and apoptosis
resultsWe found that EZH2 protein is overexpressed in approximately half of this cohort of MCL cases. More importantly, the overexpression of EZH2 is associated with poor OS in the patients. Nevertheless, simple EZH2 depletion
conclusionsOur study suggests that EZH2 participates in the pathogenesis of MCL which may serve as a potential biomarker for prognosis prediction. The dual inhibition of EZH1/2 is a promising therapeutic strategy for MCL.
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