Fen Xiong1, Yun-Zhu Mou1, Xiao-Yan Xiang2. 1. Department of Dermatology in Affiliated Hospital of North Sichuan Medical College Nanchong, Sichuan 611000, China. 2. Department of Burn Injury in Affiliated Hospital of North Sichuan Medical College Nanchong, Sichuan 637000, China.
Abstract
OBJECTIVE: As one member of the histone deacetylase inhibitor (HDACi) family, Sodium butyrate (NaB) was found out that could be used as a differentiation inducer of much cancer cell. But its effects on tumor microenvironment cells are not well recognized. The goal of this research is to investigate the effect of NaB on B16 melanoma and analysis its relevant mechanism. METHODS: We observed the effect of sodium butyrate on B16 melanoma in vivo and in vitro. MTT method was performed to detect cell apoptosis rate after treatment. Tumor associated macrophage infiltration condition was detected by flow cytometry. Western-blotting and immunohistochemical method were used to detect the expression of tumor associated macrophage cytokines. RESULTS: A certain concentration of sodium butyrate could effectively inhibit B16 melanoma growth in vivo and in vitro, and this inhibition effects related to the suppression of tumor associated macrophage differentiation. At the same time we observed the relevant macrophage factors were down-regulated compared to the control. CONCLUSION: Sodium butyrate could effectively inhibit B16 melanoma growth through suppressing tumor associated macrophage proliferation and reduce relevant pro-tumor macrophage factors expression, which may help to promote the clinical study of melanoma epigenetic therapy.
OBJECTIVE: As one member of the histone deacetylase inhibitor (HDACi) family, Sodium butyrate (NaB) was found out that could be used as a differentiation inducer of much cancer cell. But its effects on tumor microenvironment cells are not well recognized. The goal of this research is to investigate the effect of NaB on B16 melanoma and analysis its relevant mechanism. METHODS: We observed the effect of sodium butyrate on B16 melanoma in vivo and in vitro. MTT method was performed to detect cell apoptosis rate after treatment. Tumor associated macrophage infiltration condition was detected by flow cytometry. Western-blotting and immunohistochemical method were used to detect the expression of tumor associated macrophage cytokines. RESULTS: A certain concentration of sodium butyrate could effectively inhibit B16 melanoma growth in vivo and in vitro, and this inhibition effects related to the suppression of tumor associated macrophage differentiation. At the same time we observed the relevant macrophage factors were down-regulated compared to the control. CONCLUSION:Sodium butyrate could effectively inhibit B16 melanoma growth through suppressing tumor associated macrophage proliferation and reduce relevant pro-tumor macrophage factors expression, which may help to promote the clinical study of melanoma epigenetic therapy.
Authors: Daryl C Drummond; Charles O Noble; Dmitri B Kirpotin; Zexiong Guo; Gary K Scott; Christopher C Benz Journal: Annu Rev Pharmacol Toxicol Date: 2005 Impact factor: 13.820
Authors: Victor Sandor; Susan Bakke; Robert W Robey; Min H Kang; Mikhail V Blagosklonny; Jonathon Bender; Rebecca Brooks; Richard L Piekarz; Eben Tucker; William D Figg; Kenneth K Chan; Barry Goldspiel; Antonio Tito Fojo; Stanley P Balcerzak; Susan E Bates Journal: Clin Cancer Res Date: 2002-03 Impact factor: 12.531