Research Papers:

LncRNA RNCR3 promotes Chop expression by sponging miR-185-5p during MDSC differentiation

Wencong Shang, Zhenzhen Tang, Yunhuan Gao, Houbao Qi, Xiaomin Su, Yuan Zhang and Rongcun Yang _

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Oncotarget. 2017; 8:111754-111769. https://doi.org/10.18632/oncotarget.22906

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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

Correspondence to:

Rongcun Yang, email: ryang@nankai.edu.cn

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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