FATS deficiency in mice limits melanoma progression via converting the tumor immune microenvironment to the anti-tumor state
详细信息 查看官网全文
- 英文论文题名：FATS deficiency in mice limits melanoma progression via converting the tumor immune microenvironment to the anti-tumor state
- 论文作者：Zhang Lijuan ; Zhang Kai ; Wang Huafeng ; Zhang Jieyou ; Xi Qing
- 英文论文作者：Zhang Lijuan ; Zhang Kai ; Wang Huafeng ; Zhang Jieyou ; Xi Qing ; Tianjin Medical University
- 年：2016
- 作者机构：Tianjin Medical University;
- 英文论文关键词：melanoma ; FATS ; tumor immune macroenvironment ; M1 macrophage ; M2 macrophage ; NF-κB
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R739.5
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：2
- 文件大小：1323k
- 原文格式：D
- 会议级别：全国
摘要
Objective: To explore whether FATS deficiency could regulate the tumor growth and study the potential cellular and molecular mechanism.Methods: B16 melanoma cells were injected subcutaneously into FATS-/- and WT mice. We analyzed the immune microenvironment in peripheral immune organ, serum and tumor microenvironment using flow cytometry. In the in vitro study,cell differentiation, mixed cells co-culture, flow cytometry, real-time PCR and western blotting were used to further investigate the potential cellular and molecular mechanisms of FATS in tumor immunology. Finally, adoptive therapy was used to further verify the effect of FATS deficiency on melanoma.Results: We found that FATS deficiency in mice can significantly inhibit the B16 tumor growth. In addition, FATS deficiency mice obviously with increased numbers and frequency of tumor suppressor cells, including cytotoxic T lymphocyte, Th1, γδT and NK, while decreased tumor promoter cell Treg cell in tumor tissues. Notably, polarization of M1/M2 macrophage was dramatically changed in tumor tissues of the FATS deficiency mice. In our study, frequency of M1/kill macrophage significantly increased while M2/repair macrophage reduced in tumor tissues. These results showed the shift of macrophage from M2 to M1 phenotype may cause the inhibited tumor growth in FATS deficient mice. Meanwhile, FATS deficiency macrophages separated from tumor tissues facilitated T cells proliferation and increased direct tumor cytotoxicity as well. In the in vitro study, bone marrow-derived macrophages from FATS deficiency mice exhibited an intrinsic bias toward M1 polarization and increased activation of NF-κB signal pathway. Importantly, adoptive therapy of FATS-deficient macrophage significantly inhibited the growth of malenoma.Conclusion: These results demonstrated the inhibitory effect of FATS deficiency on the progression of melanoma via converting the tumor immune microenvironment to the anti-tumor state and regulating macrophage polarization in tumor immune microenvironment and suggest that FATS could be a potential immune therapeutic target for malignant tumors.
Objective: To explore whether FATS deficiency could regulate the tumor growth and study the potential cellular and molecular mechanism.Methods: B16 melanoma cells were injected subcutaneously into FATS-/- and WT mice. We analyzed the immune microenvironment in peripheral immune organ, serum and tumor microenvironment using flow cytometry. In the in vitro study,cell differentiation, mixed cells co-culture, flow cytometry, real-time PCR and western blotting were used to further investigate the potential cellular and molecular mechanisms of FATS in tumor immunology. Finally, adoptive therapy was used to further verify the effect of FATS deficiency on melanoma.Results: We found that FATS deficiency in mice can significantly inhibit the B16 tumor growth. In addition, FATS deficiency mice obviously with increased numbers and frequency of tumor suppressor cells, including cytotoxic T lymphocyte, Th1, γδT and NK, while decreased tumor promoter cell Treg cell in tumor tissues. Notably, polarization of M1/M2 macrophage was dramatically changed in tumor tissues of the FATS deficiency mice. In our study, frequency of M1/kill macrophage significantly increased while M2/repair macrophage reduced in tumor tissues. These results showed the shift of macrophage from M2 to M1 phenotype may cause the inhibited tumor growth in FATS deficient mice. Meanwhile, FATS deficiency macrophages separated from tumor tissues facilitated T cells proliferation and increased direct tumor cytotoxicity as well. In the in vitro study, bone marrow-derived macrophages from FATS deficiency mice exhibited an intrinsic bias toward M1 polarization and increased activation of NF-κB signal pathway. Importantly, adoptive therapy of FATS-deficient macrophage significantly inhibited the growth of malenoma.Conclusion: These results demonstrated the inhibitory effect of FATS deficiency on the progression of melanoma via converting the tumor immune microenvironment to the anti-tumor state and regulating macrophage polarization in tumor immune microenvironment and suggest that FATS could be a potential immune therapeutic target for malignant tumors.
Objective: To explore whether FATS deficiency could regulate the tumor growth and study the potential cellular and molecular mechanism.Methods: B16 melanoma cells were injected subcutaneously into FATS-/- and WT mice. We analyzed the immune microenvironment in peripheral immune organ, serum and tumor microenvironment using flow cytometry. In the in vitro study,cell differentiation, mixed cells co-culture, flow cytometry, real-time PCR and western blotting were used to further investigate the potential cellular and molecular mechanisms of FATS in tumor immunology. Finally, adoptive therapy was used to further verify the effect of FATS deficiency on melanoma.Results: We found that FATS deficiency in mice can significantly inhibit the B16 tumor growth. In addition, FATS deficiency mice obviously with increased numbers and frequency of tumor suppressor cells, including cytotoxic T lymphocyte, Th1, γδT and NK, while decreased tumor promoter cell Treg cell in tumor tissues. Notably, polarization of M1/M2 macrophage was dramatically changed in tumor tissues of the FATS deficiency mice. In our study, frequency of M1/kill macrophage significantly increased while M2/repair macrophage reduced in tumor tissues. These results showed the shift of macrophage from M2 to M1 phenotype may cause the inhibited tumor growth in FATS deficient mice. Meanwhile, FATS deficiency macrophages separated from tumor tissues facilitated T cells proliferation and increased direct tumor cytotoxicity as well. In the in vitro study, bone marrow-derived macrophages from FATS deficiency mice exhibited an intrinsic bias toward M1 polarization and increased activation of NF-κB signal pathway. Importantly, adoptive therapy of FATS-deficient macrophage significantly inhibited the growth of malenoma.Conclusion: These results demonstrated the inhibitory effect of FATS deficiency on the progression of melanoma via converting the tumor immune microenvironment to the anti-tumor state and regulating macrophage polarization in tumor immune microenvironment and suggest that FATS could be a potential immune therapeutic target for malignant tumors.
引文