ArticleInternational journal of medical sciences2019
Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models.
Article in International journal of medical sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Connexin-43 in Cancer: Above and Beyond Gap Junctions!Cancers · 2024Review
- Multivariate Analysis Revealed Ultrasonic-Assisted Extraction Improves Anti-Melanoma Activity of Non-Flavonoid Compounds in Indonesian Brown Algae Ethanol Extract.Molecules (Basel, Switzerland) · 2022Article
- The Influences of Omega-3 Polyunsaturated Fatty Acids on the Development of Skin Cancers.Diagnostics (Basel, Switzerland) · 2021Review
- Article
- Connexins-Therapeutic Targets in Cancers.International journal of molecular sciences · 2020Review
- The extracts ofInternational journal of medical sciences · 2019Article
Corrections and comments
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Authors and funding
9 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chemotherapy is now in common use for the treatment of tumors; however, with tumor growth retardation comes the severe side effects that occur after a chemotherapy cycle. Eicosapentaenoic acids (EPA) used in combination with chemotherapy has an additive effects and provides a rationale for using EPA in tandem with chemotherapy. To improve the efficacy and safety of this combination therapy, a further understanding that EPA modulates with the tumor microenvironment is necessary. Connexin 43 (Cx43) is involved in enhancing chemosensitivity that was suppressed in a tumor microenvironment. We aim to investigate the role of EPA in chemosensitivity in murine melanoma by inducing Cx43 expression. The dose-dependent upregulation of Cx43 expression and gap junction intercellular communication were observed in B16F10 cells after EPA treatment. Furthermore, EPA significantly increased the expression levels of mitogen-activated protein kinases (MAPK) signaling pathways. The EPA-induced Cx43 expression was reduced after MAPK inhibitors. Knockdown Cx43 in B16F10 cells reduced the therapeutic effects of combination therapy (EPA plus 5-Fluorouracil). Our results demonstrate that the treatment of EPA is a tumor induced Cx43 gap junction communication and enhances the combination of EPA and chemotherapeutic effects.
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Registered trials
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