Author/Authors :
Yang، نويسنده , , Li and Huang، نويسنده , , Jianhua and Ren، نويسنده , , Xiubao and Gorska، نويسنده , , Agnieszka E. and Chytil، نويسنده , , Anna and Aakre، نويسنده , , Mary and Carbone، نويسنده , , David P. and Matrisian، نويسنده , , Lynn M. and Richmond، نويسنده , , Ann and Lin، نويسنده , , P. Charles and Moses، نويسنده , , Harold L.، نويسنده ,
Abstract :
Summary
nt TGFβ signaling is common in human cancers and contributes to tumor metastasis. Here, we demonstrate that Gr-1+CD11b+ myeloid cells are recruited into mammary carcinomas with type II TGFβ receptor gene (Tgfbr2) deletion and directly promote tumor metastasis. Gr-1+CD11b+ cells infiltrate into the invasive front of tumor tissues and facilitate tumor cell invasion and metastasis through a process involving metalloproteinase activity. This infiltration of Gr-1+CD11b+ cells also results in increased abundance of TGFβ1 in tumors with Tgfbr2 deletion. The recruitment of Gr-1+CD11b+ cells into tumors with Tgfbr2 deletion involves two chemokine receptor axes, the SDF-1/CXCR4 and CXCL5/CXCR2 axes. Together, these data indicate that Gr-1+CD11b+ cells contribute to TGFβ-mediated metastasis through enhancing tumor cell invasion and metastasis.
