ArticleBMC cancer2020
Unphosphorylated STAT3 in heterochromatin formation and tumor suppression in lung cancer.
Article in BMC cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 38 citations in OpenAlex.
- The Prognostic Role of STAT5B Across Cancer Types and Comparative Analysis with STAT5A: A Systematic Review.Biomolecules · 2025Pooled it
- Expression and prognostic role of STAT5a across cancer types.Bioscience reports · 2023Pooled it
- Article
- STAT3-mediated suppression of the pre-induction silencer Ets-2 in activated T helper cells.Molecular biology reports · 2026Article
- Interplay between nuclear survivin and the PRC2 complex and its impact on H3K27me3-directed transcriptional repression.Journal of cell science · 2026Article
- Review
- E-cadherin endocytosis promotes non-canonical EGFR:STAT signalling to induce cell death and inhibit heterochromatinisation.PLoS genetics · 2025Article
- AhR and STAT3: A Dangerous Duo in Chemical Carcinogenesis.International journal of molecular sciences · 2025Review
- The emerging role of SARS-CoV-2 nonstructural protein 1 (nsp1) in epigenetic regulation of host gene expression.FEMS microbiology reviews · 2024Review
- NRF2 and STAT3: friends or foes in carcinogenesis?Discover oncology · 2023Review
- Moesin is an effector of tau-induced actin overstabilization, cell cycle activation, and neurotoxicity in Alzheimer's disease.iScience · 2023Article
- Chromatin and Cancer: Implications of Disrupted Chromatin Organization in Tumorigenesis and Its Diversification.Cancers · 2023Review
- Bioinformatics analysis identification ofExperimental and therapeutic medicine · 2022Article
- SHF Acts as a Novel Tumor Suppressor in Glioblastoma Multiforme by Disrupting STAT3 Dimerization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- JAK/STAT: Why choose a classical or an alternative pathway when you can have both?Journal of cellular and molecular medicine · 2022Review
- Cell Type-Specific Roles of STAT3 Signaling in the Pathogenesis and Progression of K-ras Mutant Lung Adenocarcinoma.Cancers · 2022Review
- Article
- Review
- Multilevel view on chromatin architecture alterations in cancer.Frontiers in genetics · 2022Review
- STAT proteins: a kaleidoscope of canonical and non-canonical functions in immunity and cancer.Journal of hematology & oncology · 2021Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundAberrant JAK/STAT activation has been detected in many types of human cancers. The role of JAK/STAT activation in cancer has been mostly attributed to direct transcriptional regulation of target genes by phosphorylated STAT (pSTAT), while the unphosphorylated STAT (uSTAT) is believed to be dormant and reside in the cytoplasm. However, several studies have shown that uSTATs can be found in the nucleus. In addition, it has been shown that tissue-specific loss of STAT3 or STAT5 in mice promotes cancer growth in certain tissues, and thus these STAT proteins can act as tumor suppressors. However, no unifying mechanism has been shown for the tumor suppressor function of STATs to date. We have previously demonstrated a non-canonical mode of JAK/STAT signaling for Drosophila STAT and human STAT5A, where a fraction of uSTAT is in the nucleus and associated with Heterochromatin Protein 1 (HP1); STAT activation (by phosphorylation) causes its dispersal, leading to HP1 delocalization and heterochromatin loss.
methodsWe used a combination of imaging, cell biological assays, and mouse xenografts to investigate the role of STAT3 in lung cancer development.
resultsWe found that uSTAT3 has a function in promoting heterochromatin formation in lung cancer cells, suppressing cell proliferation in vitro, and suppressing tumor growth in mouse xenografts.
conclusionsThus, uSTAT3 possesses noncanonical function in promoting heterochromatin formation, and the tumor suppressor function of STAT3 is likely attributable to the heterochromatin-promoting activity of uSTAT3 in the non-canonical JAK/STAT pathway.
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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.