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Published on: July 8, 2020
LncRNA RNCR3 promotes Chop expression by sponging miR-185-5p during MDSC differentiation
Wencong Shang1,2,3, Zhenzhen Tang1,2,3, Yunhuan Gao1,2,3
1State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Abstract:
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.
Insights
Retinal non-coding RNA3 (RNCR3) promotes myeloid-derived suppressor cell (MDSC) differentiation and immune suppression. This RNCR3/miR-185-5p/Chop network is upregulated by tumor factors, impacting cancer immunity.
Area of Science:
- Immunology
- Epigenetics
- Molecular Biology
Background:
- Myeloid-derived suppressor cells (MDSCs) are crucial regulators of immune responses in cancer and pathology.
- The precise epigenetic mechanisms governing MDSC differentiation and function remain incompletely understood.
Purpose of the Study:
- To investigate the role of retinal non-coding RNA3 (RNCR3) in MDSC differentiation and function.
- To elucidate the regulatory network involving RNCR3, miR-185-5p, and Chop in MDSCs.
Main Methods:
- Quantitative RT-PCR to assess RNCR3 and miR-185-5p expression.
- In vitro and in vivo experiments involving RNCR3 knockdown.
- Analysis of the interaction between RNCR3, miR-185-5p, and Chop.
Main Results:
- MDSCs express RNCR3, upregulated by inflammatory and tumor factors.
- RNCR3 acts as a ceRNA, promoting Chop expression by sponging miR-185-5p.
- RNCR3 knockdown inhibited MDSC differentiation and function; miR-185-5p reversed these effects by targeting Chop.
Conclusions:
- A RNCR3/miR-185-5p/Chop network promotes MDSC differentiation and suppressive function.
- This network is activated by extracellular signals, suggesting a novel therapeutic target in cancer immunology.
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