ArticleThe Kaohsiung journal of medical sciences2020
Ellagic acid induces esophageal squamous cell carcinoma cell apoptosis by modulating SHP-1/STAT3 signaling.
Article in The Kaohsiung journal of medical sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Ellagic acid is associated with reduced pancreatic carcinogenesis and modulation of the IL-6/STAT3 pathway.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2026Article
- Regulation of Matrix Metalloproteinases by Wine-Derived Compounds: Implications for Cancer Therapy.Biomolecules · 2025Review
- Exploring the Potential of Ellagic Acid in Gastrointestinal Cancer Prevention: Recent Advances and Future Directions.Oncology and therapy · 2024Review
- The potential role of plant secondary metabolites on antifungal and immunomodulatory effect.Applied microbiology and biotechnology · 2023Review
- Molecular mechanism, regulation, and therapeutic targeting of the STAT3 signaling pathway in esophageal cancer (Review).International journal of oncology · 2022Article
- RNF6 as an Oncogene and Potential Therapeutic Target-A Review.Biotech (Basel (Switzerland)) · 2020Review
- Ellagic acid induces esophageal squamous cell carcinoma cell apoptosis by modulating SHP-1/STAT3 signaling.The Kaohsiung journal of medical sciences · 2020Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Ellagic acid (EA) has been reported to have antiproliferative and antioxidant properties, but its function in esophageal squamous cell carcinoma (ESCC) has not been investigated yet. In the current study, EA was found have a significant anti-tumor activity in ESCC. In specific, EA inhibited ESCC cell survival in both of a concentration- and time-dependent manner. And our results showed that EA promoted ESCC cell apoptosis, including inducing the cleavages of PARP, and inhibiting the expression of anti-apoptotic proteins. In mechanistic, EA markedly suppressed STAT3-driven luciferase activity, and inhibited both of the endogenous and cytokines-induced STAT3 activation in ESCC cells. Further investigations indicated that EA could significantly upregulate SHP-1 expression, a negative modulator of STAT3 signaling. In contrast, knockdown of SHP-1 could attenuate the effects of EA on inhibiting ESCC cell survival. Moreover, we found that EA could inhibit RNF6 expression, an E3 of SHP-1, and overexpressing RNF6 could also significantly attenuate the effects of EA on inhibiting ESCC cell survival, which further revealed that EA could inhibit STAT3 signaling by modulating RNF6/SHP-1 axis. Our present study indicated that EA could be as a novel STAT3 inhibitor for the treatment of ESCC.
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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.