From: STING: a master regulator in the cancer-immunity cycle
Cancer types | Treatment information regarding STING activation | Biological roles of STING activation in Cancer | Reference |
---|---|---|---|
Acute meyloid leukemia | DMXAA, 450 μg, i.t. | Promote DC maturation and enhance CD8+ T cell responses via the induction of type I IFN | [44] |
Breast cancer | Topotecan (TPT, an inhibitor of topoisomerase I), 20 mg/kg, i.p. Olaparib (PARP inhibitor), 50 mg/kg daily, i.p. c-di-GMP, 150 nM, 24 h and c-di-GMP, 0.01 nM, i.p. Mafosfamide, 10 μM | Mediate DC activation Increase CD8+ T cell infiltration Activate caspase-3 and kill tumor cell directly, improve CD8+ T cell responses and restrict MDSCs Activate IFN/STAT1 pathway and protect breast cancer cells from genotoxic agents | [45] [46] [47] [48] |
Colorectal cancer | Gamma rays (6 Gy) | Induce type III IFN production after gamma-radiation by the activation of the cytosolic DNA sensors-STING-TBK1-IRF1 signaling pathway | [49] |
Radiation (40 Gy) | Promote type I IFN production and contribute to sensing irrated-tumor cells by DC Induce MDSC mobilization which mediates | [50] | |
2′3’cGAMP, 10 μg / X-ray | radioresistance in mouse models | [51] | |
Glioma | c-di-GMP, 4 μg, i.t. | Enhance CD4+ and CD8+ T cell infiltration and migration into the brain via type I IFN signaling and other chemokines | [37] |
Head and neck squamous cell carcinoma | Matrigel containing 25 μg cyclic-di-AMP (CDN) | Induce type I IFN in the host cells and promote CD8+T cell response | [52] |
cGAMP, 10 μg/ml, 24 h | Facilitate cetuximab mediated NK cell activation and DC maturation | [53] | |
R, R-CDG, 20 μg, i.t. | Promote Th1 response and increase IFN-γ+CD8+, but upregulate PD-L1 | [54] | |
R, R-CDG, 15 μg, i.t. | Increase the production of type I and II IFN but also promote the expression of PD-1 pathway components | [55] | |
Lung cancer | PARP inhibitors | Promote infiltration and activation of lymphocytes in NSCLC and SCLC | |
DMXAA/2′3’-cGAMP, 20 μg/ml, 24 h | Re-educate M2 macrophages towards an M1 phenotype in murine NSCLC | [58] | |
cGAMP, 10 μg, i.t. | Normalize tumor vasculature and augment the infiltration of CD8+ T cell in LLC tumor | [59] | |
Malignant lymphoma | 3′3’-cGAMP, 20 μM, 4 h | Induce apoptosis of malignant B cells via IRE-1/XBP-1 pathway | [60] |
Melanoma | Tumor derived DNA(B16), 1 h | Induce IFN-β production in APC and is indispensable for T cell activation and expansion | [35] |
2′3’ cGAMP, 200 nM, i.p. | Activate NK cell response | [61] | |
Nasopharyngeal carcinoma | EBV infection. | Restrict the secretion of GM-CSF and IL-6, thereby suppress the MDSC induction | [62] |
Ovary cancer | 2′3’-c-di-AM(PS) (Rp, Rp), 4 mg/kg, i.p. | Increase the infiltration of activated CD8+ T cell into tumors | [63] |
Pancreatic cancer | DMXAA, 300/450 μg, i.t. | Promote trafficking and activation of tumor-killing T cells, decrease the infiltration of Treg, and reprogram immune-suppressive macrophages | [64] |
Prostate Cancer | Cytosolic DNA generated by endonuclease MUS81 | Induce type I IFN expression and mobilize phagocytes and promote T cell responses | [65] |
c-di-GMP, 25 μg, i.t. | Provoke abscopal immunity | [66] | |
Tongue squamous cell carcinoma | HPV infection. | Enhance Treg infiltration through upregulation of CCL22 expression in HPV+ tongue squamous cells | [67] |