ArticleCancer prevention research (Philadelphia, Pa.)2011
Gambogic acid inhibits STAT3 phosphorylation through activation of protein tyrosine phosphatase SHP-1: potential role in proliferation and apoptosis.
Article in Cancer prevention research (Philadelphia, Pa.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 50 citations in OpenAlex.
- The Role of Nutraceuticals in Chemoprevention and their Therapeutic Effects when used in Combination with Synthetic Drugs.Current medicinal chemistry · 2025Review
- Review
- Gambogic Acid as a Candidate for Cancer Therapy: A Review.International journal of nanomedicine · 2020Review
- Retraction: Gambogic Acid Inhibits STAT3 Phosphorylation through Activation of Protein Tyrosine Phosphatase SHP-1: Potential Role in Proliferation and Apoptosis.Cancer prevention research (Philadelphia, Pa.) · 2018Article
- Gambogic Acid Induces Cell Apoptosis and Inhibits MAPK Pathway in PTENChinese journal of integrative medicine · 2018Article
- Molecular targets of gambogic acid in cancer: recent trends and advancements.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Review
- Recent updates of precision therapy for gastric cancer: Towards optimal tailored management.World journal of gastroenterology · 2016Review
- Inhibition of the STAT3 signaling pathway contributes to apigenin-mediated anti-metastatic effect in melanoma.Scientific reports · 2016Article
- Recent research on bioactive xanthones from natural medicine: Garcinia hanburyi.AAPS PharmSciTech · 2015Review
- Anticancer Effect and Apoptosis Induction of Gambogic Acid in Human Leukemia Cell Line K562 In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- Screening Active Compounds from Garcinia Species Native to China Reveals Novel Compounds Targeting the STAT/JAK Signaling Pathway.BioMed research international · 2015Article
- Alterations of cell cycle control proteins SHP‑1/2, p16, CDK4 and cyclin D1 in radioresistant nasopharyngeal carcinoma cells.Molecular medicine reports · 2014Article
- SHP1-mediated cell cycle redistribution inhibits radiosensitivity of non-small cell lung cancer.Radiation oncology (London, England) · 2013Article
- New targets for the antitumor activity of gambogic acid in hematologic malignancies.Acta pharmacologica Sinica · 2013Review
- Novel sorafenib analogues induce apoptosis through SHP-1 dependent STAT3 inactivation in human breast cancer cells.Breast cancer research : BCR · 2013Article
- Effects of gambogic acid on the activation of caspase-3 and downregulation of SIRT1 in RPMI-8226 multiple myeloma cells via the accumulation of ROS.Oncology letters · 2012Article
Corrections and comments
- Retraction · 2018-09-04Author Unresponsive · Concerns/Issues about Data · Duplication of/in Image · Investigation by Company/Institution · Manipulation of Images ·
- Retracted
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transcription factor, STAT3, is associated with proliferation, survival, and metastasis of cancer cells. We investigated whether gambogic acid (GA), a xanthone derived from the resin of traditional Chinese medicine, Garcinia hanburyi (mangosteen), can regulate the STAT3 pathway, leading to suppression of growth and sensitization of cancer cells. We found that GA induced apoptosis in human multiple myeloma cells that correlated with the inhibition of both constitutive and inducible STAT3 activation. STAT3 phosphorylation at both tyrosine residue 705 and serine residue 727 was inhibited by GA. STAT3 suppression was mediated through the inhibition of activation of the protein tyrosine kinases Janus-activated kinase 1 (JAK1) and JAK2. Treatment with the protein tyrosine phosphatase (PTP) inhibitor pervanadate reversed the GA-induced downregulation of STAT3, suggesting the involvement of a PTP. We also found that GA induced the expression of the PTP SHP-1. Deletion of the SHP-1 gene by siRNA suppressed the ability of GA to inhibit STAT3 activation and to induce apoptosis, suggesting the critical role of SHP-1 in its action. Moreover, GA downregulated the expression of STAT3-regulated antiapoptotic (Bcl-2, Bcl-xL, and Mcl-1), proliferative (cyclin D1), and angiogenic (VEGF) proteins, and this correlated with suppression of proliferation and induction of apoptosis. Overall, these results suggest that GA blocks STAT3 activation, leading to suppression of tumor cell proliferation and induction of apoptosis.
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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.