ArticleProceedings of the National Academy of Sciences of the United States of America2013
STAT3 suppresses transcription of proapoptotic genes in cancer cells with the involvement of its N-terminal domain.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed, 140 citations in OpenAlex.
- STAT3-mediated suppression of the pre-induction silencer Ets-2 in activated T helper cells.Molecular biology reports · 2026Article
- The novel agent VP79s synergistically enhances venetoclax activity in multiple myeloma cells.Investigational new drugs · 2026Article
- ERK1/2 hijack STAT3 via Thr714 phosphorylation to suppress gene expression.Cell communication and signaling : CCS · 2026Article
- STAT3 signaling in cancer: mechanisms and targeting therapeutic.Frontiers in immunology · 2026Review
- JI017 induces cell line specific anticancer effects in hepatocellular carcinoma by suppressing the STAT3 signaling pathway.Molecular biology reports · 2025Article
- STAT3: Key targets of growth-promoting receptor positive breast cancer.Cancer cell international · 2024Review
- Signaling pathways in liver cancer: pathogenesis and targeted therapy.Molecular biomedicine · 2024Review
- Vaccinia Virus: Mechanisms Supporting Immune Evasion and Successful Long-Term Protective Immunity.Viruses · 2024Review
- Exploring Novel Frontiers: Leveraging STAT3 Signaling for Advanced Cancer Therapeutics.Cancers · 2024Review
- Unraveling the complexity of STAT3 in cancer: molecular understanding and drug discovery.Journal of experimental & clinical cancer research : CR · 2024Review
- Exploring molecular targets in cancer: Unveiling the anticancer potential of Paeoniflorin through a comprehensive analysis of diverse signaling pathways and recent advances.Journal of biological methods · 2024Review
- JAK/STAT3 signaling in cardiac fibrosis: a promising therapeutic target.Frontiers in pharmacology · 2024Review
- The mechanisms of tanshinone in the treatment of tumors.Frontiers in pharmacology · 2023Review
- Role of STAT3 and NRF2 in Tumors: Potential Targets for Antitumor Therapy.Molecules (Basel, Switzerland) · 2022Review
- Emerging roles of circular RNAs in gastric cancer metastasis and drug resistance.Journal of experimental & clinical cancer research : CR · 2022Review
- Nobiletin as an inducer of programmed cell death in cancer: a review.Apoptosis : an international journal on programmed cell death · 2022Review
- Anticarin-Acta pharmaceutica Sinica. B · 2022Article
- Niraparib-induced STAT3 inhibition increases its antitumor effects.Frontiers in oncology · 2022Article
- Article
- Paeoniflorin Regulates NEDD4L/STAT3 Pathway to Induce Ferroptosis in Human Glioma Cells.Journal of oncology · 2022Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Activation of STAT3 in cancers leads to gene expression promoting cell proliferation and resistance to apoptosis, as well as tumor angiogenesis, invasion, and migration. In the characterization of effects of ST3-H2A2, a selective inhibitor of the STAT3 N-terminal domain (ND), we observed that the compound induced apoptotic death in cancer cells associated with robust activation of proapoptotic genes. Using ChIP and tiling human promoter arrays, we found that activation of gene expression in response to ST3-H2A2 is accompanied by altered STAT3 chromatin binding. Using inhibitors of STAT3 phosphorylation and a dominant-negative STAT3 mutant, we found that the unphosphorylated form of STAT3 binds to regulatory regions of proapoptotic genes and prevents their expression in tumor cells but not normal cells. siRNA knockdown confirmed the effects of ST3-HA2A on gene expression and chromatin binding to be STAT3 dependent. The STAT3-binding region of the C/EBP-homologous protein (CHOP) promoter was found to be localized in DNaseI hypersensitive site of chromatin in cancer cells but not in nontransformed cells, suggesting that STAT3 binding and suppressive action can be chromatin structure dependent. These data demonstrate a suppressive role for the STAT3 ND in the regulation of proapoptotic gene expression in cancer cells, providing further support for targeting STAT3 ND for cancer therapy.
Indexed as
Identifiers
What OpenQuestion holds
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.