LncRNA RNCR3 promotes Chop expression by sponging miR-185-5p during MDSC differentiation
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Wencong Shang1,2,3, Zhenzhen Tang1,2,3, Yunhuan Gao1,2,3, Houbao Qi1,2,3, Xiaomin Su1,2,3, Yuan Zhang1,2,3 and Rongcun Yang1,2,3
1State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China
2Key Laboratory of Bioactive Materials, Ministry of Education, Nankai University, Tianjin, China
3Department of Immunology, Nankai University School of Medicine, Nankai University, Tianjin, China
Rongcun Yang, email: email@example.com
Keywords: myeloid-derived suppressor cells; RNCR3; miR-185-5p; Chop; epigenetic modification
Received: July 13, 2017 Accepted: November 17, 2017 Published: December 04, 2017
Myeloid-derived suppressor cells (MDSCs) play a critical role in regulating immune responses in cancer and other pathological conditions. Mechanism(s) regulating MDSC differentiation and function is not completely clear, especially epigenetic regulation. In this study, we found that MDSCs express retinal non-coding RNA3 (RNCR3), and the expression in MDSCs is upregulated by inflammatory and tumor associated factors. RNCR3 may function as a competing endogenous RNA (ceRNA) to promote Chop expression by sponging miR-185-5p during MDSC differentiation. RNCR3 knockdown suppressed differentiation and function of MDSCs in vitro and in vivo. Quantitative RT-PCR showed that RNCR3 was negatively regulated by miR-185-5p in MDSCs. MiR-185-5p affected the expansion of MDSCs and reversed the effect of RNCR3 on MDSC differentiation and function through directly targeting Chop. Thus, our results suggest a RNCR3/miR-185-5p/Chop autologously strengthening network to promote MDSC differentiation and suppressive function in response to extracellular inflammatory and tumor-associated signals.
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