ArticleCancer science2019
Epigenetic silencing of SOCS5 potentiates JAK-STAT signaling and progression of T-cell acute lymphoblastic leukemia.
Article in Cancer science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 42 citations in OpenAlex.
- Sequential inspiratory muscle exercise-noninvasive positive pressure ventilation alleviates oxidative stress in COPD by mediating SOCS5/JAK2/STAT3 pathway.BMC pulmonary medicine · 2023Trial
- Epigenetic drift score captures directional methylation variability and links aging to transcriptional, metabolic, and genetic alterations.Genome research · 2025Article
- Transcriptomic profiles of susceptibility and resilience to stress in the amygdala and hippocampus of male rats.Neurobiology of stress · 2025Article
- SOCS5, targeted by miR-155-5p, plays a negative regulatory role in pulmonary hypertension through inhibiting JAK2/STAT3 signaling pathway.BMC pulmonary medicine · 2024Article
- Prognostic impact ofTherapeutic advances in hematology · 2024Article
- Thyroid hormone T3 induces Fyn modification and modulates palmitoyltransferase gene expression through αvβ3 integrin receptor in PC12 cells during hypoxia.Translational neuroscience · 2024Article
- Unravelling the druggability and immunological roles of the SOCS-family proteins.Frontiers in immunology · 2024Review
- Challenges and Future Trends in Atopic Dermatitis.International journal of molecular sciences · 2023Review
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
- Multiomics to investigate the mechanisms contributing to repression of PTPRC and SOCS2 in pediatric T-ALL: Focus on miR-363-3p and promoter methylation.Genes, chromosomes & cancer · 2022Article
- LncRNA small nucleolar RNA host gene 16 reduces sepsis-induced myocardial damage by regulating miR-421/suppressor of cytokine signaling 5 axis.The Kaohsiung journal of medical sciences · 2022Article
- T-Cell Acute Lymphoblastic Leukemia-Current Concepts in Molecular Biology and Management.Biomedicines · 2021Review
- The Emerging Role of Suppressors of Cytokine Signaling (SOCS) in the Development and Progression of Leukemia.Cancers · 2021Review
- The LINC01119-SOCS5 axis as a critical theranostic in triple-negative breast cancer.NPJ breast cancer · 2021Article
- Deregulation of the Interleukin-7 Signaling Pathway in Lymphoid Malignancies.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Leonurine-Repressed miR-18a-5p/SOCS5/JAK2/STAT3 Axis Activity Disrupts CML malignancy.Frontiers in pharmacology · 2021Article
- The Role of Janus Kinase/STAT3 Pathway in Hematologic Malignancies With an Emphasis on Epigenetics.Frontiers in genetics · 2021Review
- Fraxetin Inhibits the Proliferation and Metastasis of Glioma Cells by Inactivating JAK2/STAT3 Signaling.Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Article
- The overexpression of miRNA-212-5p inhibited the malignant proliferation of liver cancer cells HepG2 and the tumor formation in nude mice with transplanted tumor through down-regulating SOCS5.Translational cancer research · 2020Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Activating mutations in cytokine receptors and transcriptional regulators govern aberrant signal transduction in T-cell lineage acute lymphoblastic leukemia (T-ALL). However, the roles played by suppressors of cytokine signaling remain incompletely understood. We examined the regulatory roles of suppressor of cytokine signaling 5 (SOCS5) in T-ALL cellular signaling networks and leukemia progression. We found that SOCS5 was differentially expressed in primary T-ALL and its expression levels were lowered in HOXA-deregulated leukemia harboring KMT2A gene rearrangements. Here, we report that SOCS5 expression is epigenetically regulated by DNA methyltransferase-3A-mediated DNA methylation and methyl CpG binding protein-2-mediated histone deacetylation. We show that SOCS5 negatively regulates T-ALL cell growth and cell cycle progression but has no effect on apoptotic cell death. Mechanistically, SOCS5 silencing induces activation of JAK-STAT signaling, and negatively regulates interleukin-7 and interleukin-4 receptors. Using a human T-ALL murine xenograft model, we show that genetic inactivation of SOCS5 accelerates leukemia engraftment and progression, and leukemia burden. We postulate that SOCS5 is epigenetically deregulated in T-ALL and serves as an important regulator of T-ALL cell proliferation and leukemic progression. Our results link aberrant downregulation of SOCS5 expression to the enhanced activation of the JAK-STAT and cytokine receptor-signaling cascade in T-ALL.
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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.