Jun Ren
Chongqing Medical University
3 Papers
Jun Ren is an academic researcher from Chongqing Medical University. The author has contributed to research in topics: Autophagy & Myeloid leukemia. The author has an hindex of 1, co-authored 3 publications.
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Papers
Tumour-derived small extracellular vesicles suppress CD8+ T cell immune function by inhibiting SLC6A8-mediated creatine import in NPM1-mutated acute myeloid leukaemia.
Meixi Peng,Jun Ren,Yipei Jing,Xueke Jiang,Qiaoling Xiao,Junpeng Huang,Yonghong Tao,Li Lei,Xin Wang,Zailin Yang,Zailin Yang,Zesong Yang,Qian Zhan,Can Lin,Guoxiang Jin,Xian Zhang,Ling Zhang +16 more
TL;DR: In this paper, leukemic cells secreted miR-19a-3p into the tumour microenvironment via small extracellular vesicles (sEVs), which was controlled by the NPM1-mutated protein/CCCTC-binding factor (CTCF)/poly (A)-binding protein cytoplasmic 1 (PABPC1) signalling axis.
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NPM1 mutant maintains ULK1 protein stability via TRAF6-dependent ubiquitination to promote autophagic cell survival in leukemia.
Yuting Tang,Yao Tao,Lu Wang,Liyuan Yang,Yipei Jing,Xueke Jiang,Li Lei,Zailin Yang,Xin Wang,Meixi Peng,Qiaoling Xiao,Jun Ren,Ling Zhang +12 more
TL;DR: It is suggested that NPM1 mutant interacts with ULK1, and thus, maintains its protein stability, which is required for N PM1 mutant‐mediated autophagic cell survival, and this data extend the understanding of the functions of NPM2 mutant in the regulation of autophagy activation in NPM 1‐mutated AML.
Mutant NPM1-regulated lncRNA HOTAIRM1 promotes leukemia cell autophagy and proliferation by targeting EGR1 and ULK3.
Yipei Jing,Xueke Jiang,Li Lei,Meixi Peng,Jun Ren,Qiaoling Xiao,Yao Tao,Yonghong Tao,Junpeng Huang,Lu Wang,Yuting Tang,Zailin Yang,Zesong Yang,Ling Zhang +13 more
Abstract: Background Acute myeloid leukemia (AML) with mutated nucleophosmin (NPM1), which displays a distinct long noncoding RNA (lncRNA) expression profile, has been defined as a unique subgroup in the new classification of myeloid neoplasms. However, the biological roles of key lncRNAs in the development of NPM1-mutated AML are currently unclear. Here, we aimed to investigate the functional and mechanistic roles of the lncRNA HOTAIRM1 in NPM1-mutated AML. Methods The expression of HOTAIRM1 was analyzed with a public database and further determined by qRT-PCR in NPM1-mutated AML samples and cell lines. The cause of upregulated HOTAIRM1 expression was investigated by luciferase reporter, chromatin immunoprecipitation and ubiquitination assays. The functional role of HOTAIRM1 in autophagy and proliferation was evaluated using western blot analysis, immunofluorescence staining, a Cell Counting Kit-8 (CCK-8) assay, a 5-ethynyl-2'-deoxyuridine (EdU) incorporation assay, flow cytometric analyses and animal studies. The action mechanism of HOTAIRM1 was explored through RNA fluorescence in situ hybridization, RNA pulldown and RNA immunoprecipitation assays. Results HOTAIRM1 was highly expressed in NPM1-mutated AML. High HOTAIRM1 expression was induced in part by mutant NPM1 via KLF5-dependent transcriptional regulation. Importantly, HOTAIRM1 promoted autophagy and proliferation both in vitro and in vivo. Mechanistic investigations demonstrated that nuclear HOTAIRM1 promoted EGR1 degradation by serving as a scaffold to facilitate MDM2-EGR1 complex formation, while cytoplasmic HOTAIRM1 acted as a sponge for miR-152-3p to increase ULK3 expression. Conclusions Taken together, our findings identify two oncogenic regulatory axes in NPM1-mutated AML centered on HOTAIRM1: one involving EGR1 and MDM2 in the nucleus and the other involving the miR-152-3p/ULK3 axis in the cytoplasm. Our study indicates that HOTAIRM1 may be a promising therapeutic target for this distinct leukemia subtype.