| First Author | Zhu H | Year | 2017 |
| Journal | J Exp Clin Cancer Res | Volume | 36 |
| Issue | 1 | Pages | 2 |
| PubMed ID | 28057020 | Mgi Jnum | J:288201 |
| Mgi Id | MGI:6430871 | Doi | 10.1186/s13046-016-0471-3 |
| Citation | Zhu H, et al. (2017) RNA virus receptor Rig-I monitors gut microbiota and inhibits colitis-associated colorectal cancer. J Exp Clin Cancer Res 36(1):2 |
| abstractText | BACKGROUND: Retinoic acid-inducible gene-I (Rig-I) is an intracellular viral RNA receptor, which specifically recognizes double-stranded viral RNA initiating antiviral innate immunity. Increasing evidences showed that Rig-I had broader roles in antibacterial immunity and cancer protection. However, the potential roles and mechanisms of Rig-I in gut flora regulation and colorectal cancer (CRC) progression remain unclear. METHODS: Immunohistochemistry was performed to detect Rig-I protein in 38 pairs of CRC tissue and matched adjacent mucosa, and immunofluorescence and western blot were also used to detect Rig-I protein expression in AOM/DSS-induced mice CRC samples. High-throughput sequencing was conducted to evaluate gut microbiota changes in Rig-I-deficient mice. Immunofluorescence and flow cytometry were used to detect IgA expression. Additionally, real-time quantitative PCR was performed to detect RNA expression in mouse intestines and cultured cells, and western blot was used to detect phosphorylation of STAT3 in IL-6-stimulated B cell line. RESULTS: Rig-I was downregulated in human and mouse CRC samples and Rig-I-deficient mice were more susceptible to AOM/DSS-induced colitis-associated colorectal cancer (CAC). Furthermore, Rig-I-deficient mice displayed gut microbiota disturbance compared to wild type mice. IgA, Reg3gamma and Pdcd1 levels were decreased in intestines of Rig-I-deficient mice. Phosphorylation of STAT3 in IL-6-stimulated 1B4B6 was decreased. CONCLUSION: Rig-I could regulate gut microbiota through regulating IgA and IL6-STAT3-dependent Reg3gamma expression. Besides, Rig-I could inhibit CRC progression. |
