title: Tumor apoptosis by indole-3-acetic acid/light in B16F10 melanoma-implanted nude mice.
abstract: Recently, we reported that UVB-activated indole-3-acetic acid (IAA) induces the apoptosis of G361 human melanoma cells. In the present study, we used IAA and visible light combinations to treat B16F10 melanoma-implanted nude mice using an experimental intense pulsed light (IPL) therapy model. We first investigated whether activated IAA by horseradish peroxidase (HRP) or UVB causes apoptosis of B16F10 melanoma cells. IAA/HRP or IAA/UVB combination lead to apoptosis of B16F10 cells, as reported in other cell lines. Interestingly, IAA alone was not cytotoxic. These findings suggested the potential use of IAA in the treatment of melanoma. For the future clinical use, we also tested whether visible light has the same effects like UVB and found that visible light also activates IAA to produce free radicals and that IAA/visible light decreased cell viability significantly. Based on these results, IAA/IPL combination was tried whether it can induce apoptosis in vivo status. TUNEL staining showed that IAA/IPL treatment induced apoptosis of tumor cells. In addition, the expressions of p53, Fas, and PARP were upregulated in the IAA/IPL-treated group than in untreated control, demonstrating that IAA/IPL treatment caused apoptosis in melanoma-implanted nude mice. In conclusion, we showed that IAA/IPL induces melanoma regression in B16F10 melanoma-implanted nude mice. These results suggest the potential use of IAA/IPL in the treatment of malignant melanoma.
authors.affiliation: Department of Biochemistry, College of Medicine, Chung-Ang University, 221 Heukseok-Dong Dongjak-Gu, Seoul 156-756, Republic of Korea.
authors.forename: So-Young
authors.initials: SY
authors.lastname: Kim
authors.forename: Myo-Kyoung
authors.initials: MK
authors.lastname: Kim
authors.forename: Sun-Bang
authors.initials: SB
authors.lastname: Kwon
authors.forename: Jung-Im
authors.initials: JI
authors.lastname: Na
authors.forename: Kyoung-Chan
authors.initials: KC
authors.lastname: Park
authors.forename: Dong-Seok
authors.initials: DS
authors.lastname: Kim
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects; D005609:Free Radicals / Q000378:metabolism; D006735:Horseradish Peroxidase / Q000378:metabolism; D007210:Indoleacetic Acids / Q000378:metabolism*; D008027:Light; D008546:Melanoma, Experimental / Q000235:genetics / Q000473:pathology*; D051379:Mice; D008819:Mice, Nude; D009368:Neoplasm Transplantation; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases / Q000235:genetics / Q000378:metabolism; D047368:Tumor Burden / Q000187:drug effects / Q000528:radiation effects; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects / Q000528:radiation effects; D019014:fas Receptor / Q000235:genetics / Q000378:metabolism
chemical_list: C491899:Fas protein, mouse; D005609:Free Radicals; D007210:Indoleacetic Acids; D016159:Tumor Suppressor Protein p53; D019014:fas Receptor; C030737:indoleacetic acid; D006735:Horseradish Peroxidase; C499321:Parp1 protein, mouse; D000071137:Poly (ADP-Ribose) Polymerase-1; D011065:Poly(ADP-ribose) Polymerases