Your browser doesn't support javascript.
loading
GCH1 induces immunosuppression through metabolic reprogramming and IDO1 upregulation in triple-negative breast cancer.
Wei, Jin-Li; Wu, Si-Yu; Yang, Yun-Song; Xiao, Yi; Jin, Xi; Xu, Xiao-En; Hu, Xin; Li, Da-Qiang; Jiang, Yi-Zhou; Shao, Zhi-Ming.
Afiliación
  • Wei JL; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Wu SY; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Yang YS; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Xiao Y; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Jin X; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Xu XE; Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Hu X; Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Li DQ; Cancer Institute, Fudan University Shanghai Cancer Center, Shanghai, China.
  • Jiang YZ; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China zhimingshao@yahoo.com yizhoujiang@fudan.edu.cn.
  • Shao ZM; Department of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai, China zhimingshao@yahoo.com yizhoujiang@fudan.edu.cn.
J Immunother Cancer ; 9(7)2021 07.
Article en En | MEDLINE | ID: mdl-34281987
PURPOSE: Regulatory T cells (Tregs) heavily infiltrate triple-negative breast cancer (TNBC), and their accumulation is affected by the metabolic reprogramming in cancer cells. In the present study, we sought to identify cancer cell-intrinsic metabolic modulators correlating with Tregs infiltration in TNBC. EXPERIMENTAL DESIGN: Using the RNA-sequencing data from our institute (n=360) and the Molecular Taxonomy of Breast Cancer International Consortium TNBC cohort (n=320), we calculated the abundance of Tregs in each sample and evaluated the correlation between gene expression levels and Tregs infiltration. Then, in vivo and in vitro experiments were performed to verify the correlation and explore the underlying mechanism. RESULTS: We revealed that GTP cyclohydrolase 1 (GCH1) expression was positively correlated with Tregs infiltration and high GCH1 expression was associated with reduced overall survival in TNBC. In vivo and in vitro experiments showed that GCH1 increased Tregs infiltration, decreased apoptosis, and elevated the programmed cell death-1 (PD-1)-positive fraction. Metabolomics analysis indicated that GCH1 overexpression reprogrammed tryptophan metabolism, resulting in L-5-hydroxytryptophan (5-HTP) accumulation in the cytoplasm accompanied by kynurenine accumulation and tryptophan reduction in the supernatant. Subsequently, aryl hydrocarbon receptor, activated by 5-HTP, bound to the promoter of indoleamine 2,3-dioxygenase 1 (IDO1) and thus enhanced the transcription of IDO1. Furthermore, the inhibition of GCH1 by 2,4-diamino-6-hydroxypyrimidine (DAHP) decreased IDO1 expression, attenuated tumor growth, and enhanced the tumor response to PD-1 blockade immunotherapy. CONCLUSIONS: Tumor-cell-intrinsic GCH1 induced immunosuppression through metabolic reprogramming and IDO1 upregulation in TNBC. Inhibition of GCH1 by DAHP serves as a potential immunometabolic strategy in TNBC.
Asunto(s)
Palabras clave

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Reguladores / Indolamina-Pirrol 2,3,-Dioxigenasa / Neoplasias de la Mama Triple Negativas / GTP Ciclohidrolasa Límite: Animals / Female / Humans Idioma: En Revista: J Immunother Cancer Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Linfocitos T Reguladores / Indolamina-Pirrol 2,3,-Dioxigenasa / Neoplasias de la Mama Triple Negativas / GTP Ciclohidrolasa Límite: Animals / Female / Humans Idioma: En Revista: J Immunother Cancer Año: 2021 Tipo del documento: Article País de afiliación: China Pais de publicación: Reino Unido