长链非编码RNA RNCR3在髓源性抑制细胞分化过程中通过吸附miR-185-5p促进Chop表达。
LncRNA RNCR3 promotes Chop expression by sponging miR-185-5p during MDSC differentiation.
作者信息
Shang Wencong, Tang Zhenzhen, Gao Yunhuan, Qi Houbao, Su Xiaomin, Zhang Yuan, Yang Rongcun
机构信息
State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
Key Laboratory of Bioactive Materials, Ministry of Education, Nankai University, Tianjin, China.
出版信息
Oncotarget. 2017 Dec 4;8(67):111754-111769. doi: 10.18632/oncotarget.22906. eCollection 2017 Dec 19.
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 and . 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.
髓源性抑制细胞（MDSCs）在癌症和其他病理状态下调节免疫反应中发挥关键作用。调节MDSC分化和功能的机制尚不完全清楚，尤其是表观遗传调控。在本研究中，我们发现MDSCs表达视网膜非编码RNA3（RNCR3），且MDSCs中的表达受炎症和肿瘤相关因子上调。在MDSC分化过程中，RNCR3可能作为一种竞争性内源性RNA（ceRNA），通过海绵吸附miR-185-5p来促进Chop表达。敲低RNCR3可抑制MDSCs的分化和功能。定量逆转录聚合酶链反应显示，在MDSCs中RNCR3受miR-185-5p负调控。MiR-185-5p影响MDSCs的扩增，并通过直接靶向Chop逆转RNCR3对MDSC分化和功能的影响。因此，我们的结果提示存在一个RNCR3/miR-185-5p/Chop自身强化网络，以促进MDSC分化和抑制功能，从而响应细胞外炎症和肿瘤相关信号。
Zotero 插件