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  • microRNA-155 deficiency impairs dendritic cell function in breast cancer.

microRNA-155 deficiency impairs dendritic cell function in breast cancer.

Oncoimmunology (2016-12-22)
Junfeng Wang, Stephen Iwanowycz, Fang Yu, Xuemei Jia, Shuilong Leng, Yuzhen Wang, Wei Li, Shiang Huang, Walden Ai, Daping Fan
摘要

In antitumor immunity, dendritic cells (DCs) capture, process, and present tumor antigens to T cells, initiating a tumoricidal response. However, DCs are often dysfunctional due to their exposure to the tumor microenvironment (TME), leading to tumor escape from immune surveillance. Here, a vital role of microRNA-155 (miR-155) in regulating the function of DCs in breast cancer is reported. Host miR-155 deficiency enhanced breast cancer growth in mice, accompanied by reduced DCs in the tumors and draining lymph nodes. miR-155 deficiency in DCs impaired their maturation, migration ability, cytokine production, and the ability to activate T cells. We demonstrate that miR-155 regulates DC migration through epigenetic modulation of CCR7 expression. Moreover, IL-6 and IL-10, two cytokines abundant in the TME, are found to impair DC maturation by suppressing miR-155 expression. Furthermore, animal studies show that a lack of miR-155 diminishes the effectiveness of DC-based immunotherapy for breast cancer. In conclusion, these findings suggest that miR-155 is a master regulator of DC function in breast cancer, including maturation, cytokine secretion, migration toward lymph nodes, and activation of T-cells. These results suggest that boosting the expression of a single microRNA, miR-155, may significantly improve the efficacy of DC-based immunotherapies for breast cancer.

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Roche
红细胞裂解液, solution, Roche, pkg of 100 mL, sufficient for 50-500 reactions
Sigma-Aldrich
山羊抗兔IgG抗体,过氧化物酶偶联, 1 mg/mL (after reconstitution), Chemicon®