Publication: Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models
Issued Date
2019-01-01
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ISSN
14491907
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2-s2.0-85067099569
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Mahidol University
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SCOPUS
Bibliographic Citation
International Journal of Medical Sciences. Vol.16, No.5 (2019), 636-643
Suggested Citation
Chih Jen Yang, Chi Te Kuo, Li Hsien Wu, Man Chin Chen, Christian Ronquillo Pangilinan, Naphichaya Phacharapiyangkul, Wangta Liu, Ya Huey Chen, Che Hsin Lee Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models. International Journal of Medical Sciences. Vol.16, No.5 (2019), 636-643. doi:10.7150/ijms.30889 Retrieved from: https://repository.li.mahidol.ac.th/handle/20.500.14594/52383
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Title
Eicosapentaenoic acids enhance chemosensitivity through connexin 43 upregulation in murine melanoma models
Abstract
© Ivyspring International Publisher. 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.