ArticleThe American journal of pathology2009
Epigenetic silencing of Stk39 in B-cell lymphoma inhibits apoptosis from genotoxic stress.
Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 23 citations in OpenAlex.
- Knockdown of STK39 inhibits lung cancer brain metastasis by suppressing the CPSF4/NFκB/COX2 pathway.Journal of neuro-oncology · 2025Article
- Article
- DNA Methylation Changes in Autologous Hematopoietic Stem Cell Transplant Patients.Biological research for nursing · 2023Article
- Discovery of synthetic lethal and tumor suppressor paralog pairs in the human genome.Cell reports · 2021Article
- Identifying Methylation Pattern and Genes Associated with Breast Cancer Subtypes.International journal of molecular sciences · 2019Article
- Tumor-associated antigens identified early in mouse mammary tumor development can be effective vaccine targets.Vaccine · 2019Article
- Epstein-Barr Virus (EBV) Latent Protein EBNA3A Directly Targets and Silences theJournal of virology · 2018Article
- STK39 blockage by RNA interference inhibits the proliferation and induces the apoptosis of renal cell carcinoma.OncoTargets and therapy · 2018Article
- STK39, overexpressed in osteosarcoma, regulates osteosarcoma cell invasion and proliferation.Oncology letters · 2017Article
- An epigenome-wide study of body mass index and DNA methylation in blood using participants from the Sister Study cohort.International journal of obesity (2005) · 2017Article
- Role of high expression levels of STK39 in the growth, migration and invasion of non-small cell type lung cancer cells.Oncotarget · 2016Article
- Galectin-1 regulates tissue exit of specific dendritic cell populations.The Journal of biological chemistry · 2015Article
- The International SSRI Pharmacogenomics Consortium (ISPC): a genome-wide association study of antidepressant treatment response.Translational psychiatry · 2015Article
- Persistence of furan-induced epigenetic aberrations in the livers of F344 rats.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Actions of the protein kinase WNK1 on endothelial cells are differentially mediated by its substrate kinases OSR1 and SPAK.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Identification of the genomic insertion site of Pmel-1 TCR α and β transgenes by next-generation sequencing.PloS one · 2014Article
- Differential transcriptomic analysis of spontaneous lung tumors in B6C3F1 mice: comparison to human non-small cell lung cancer.Toxicologic pathology · 2012Article
- Molecular physiology of SPAK and OSR1: two Ste20-related protein kinases regulating ion transport.Physiological reviews · 2012Review
- Repression of the DNA-binding inhibitor Id3 by Blimp-1 limits the formation of memory CD8+ T cells.Nature immunology · 2011Article
- New developments in the pathology of malignant lymphoma: a review of the literature published from August to November 2009.Journal of hematopathology · 2009Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
B-cell lymphomas, the most frequent human immune system malignancies, often contain dysregulated TCL1 oncogene expression. TCL1 transgenic (TCL1-tg) mice develop a spectrum of B-cell malignancies, supporting an oncogenic role for TCL1 in B cells. Our prior global survey of DNA methylation patterns in TCL1-tg B-cell lymphomas identified many lymphoma-specific candidate hypermethylated genes, including Stk39. The Stk39 encoded protein, sterile 20-like-related proline-alanine-rich kinase (SPAK), regulates cell stress responses, and microarray studies identified reduced SPAK expression in metastatic prostate and treatment-resistant breast cancers, suggesting that its loss may have a role in cancer progression. Here we identified DNA hypermethylation and SPAK silencing in TCL1-tg B-cell lymphomas and SPAK silencing without DNA methylation in multiple subtypes of human B-cell lymphomas. SPAK knockdown by shRNA protected B cells from caspase-dependent apoptosis induced by DNA double-strand breaks but not apoptosis in response to osmotic or oxidative cell stressors. Caspase 3 activation by cleavage was impaired with SPAK repression in DNA damaged B cells. Interestingly, c-Jun NH(2)-terminal kinase is potentially activated by SPAK and pharmacological inhibition of c-Jun NH(2)-terminal kinase in SPAK-expressing B cells recapitulated the cell-protective phenotype of SPAK knockdown. Taken together, these data indicate that SPAK loss in B-cell lymphomas promotes increased cell survival with DNA damage and provides a potential mechanism for increased resistance to genotoxic stress in cancer.
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