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长链非编码 RNA USP30-AS1 通过顺式调控 USP30 和 ANKRD13A 促进急性髓系白血病细胞的存活。

LncRNA USP30-AS1 promotes the survival of acute myeloid leukemia cells by cis-regulating USP30 and ANKRD13A.

机构信息

Department of Hematology, School of Medicine, Guangzhou First People's Hospital, South China University of Technology, Guangzhou, Guangdong, China.

出版信息

Hum Cell. 2022 Jan;35(1):360-378. doi: 10.1007/s13577-021-00636-7. Epub 2021 Oct 25.

DOI:10.1007/s13577-021-00636-7
PMID:34694569
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8732929/
Abstract

Acute myeloid leukemia (AML) is a malignant tumor derived from leukemia stem cells, with complicated pathogenesis. LncRNAs play an important role in tumors genesis and progression. According to results from bioinformatics analysis, lncRNA USP30-AS1 is highly expressed in AML and both the high expression of USP30-AS1 and low methylation level at Cg03124318 locus of USP30-AS1 gene promoter are associated with poor prognosis of AML. This study knocked down and overexpressed USP30-AS1 to determine the roles in AML cell lines. High-throughput sequencing was performed to explore the genes regulated by USP30-AS1. Results showed that USP30-AS1 promoted AML cell viability and inhibited apoptosis. Genes regulated by USP30-AS1 are mainly related to genetic regulation and immune system. Among them, USP30 and ANKRD13A genes are close to USP30-AS1 gene in chromosome. Knockdown of USP30, but not ANKRD13A, abolished the cancer-promoting effects of USP30-AS1. ANKRD13A recognizes Lys-63-linked polyubiquitin chain in HLA-I. USP30-AS1 induced HLA-I internalization from the cell membrane by up-regulating ANKRD13A, which might induce the immune escape of AML cells. ChIP analysis revealed that the regulatory effects of USP30-AS1 on USP30 and ANKRD13A are associated with H3K4me3 and H3K27Ac. In summary, USP30-AS1 probably promotes AML cell survival by cis-regulating USP30 and ANKRD13A.

摘要

急性髓细胞白血病（AML）是一种起源于白血病干细胞的恶性肿瘤，其发病机制复杂。长链非编码 RNA（lncRNA）在肿瘤的发生和发展中发挥重要作用。根据生物信息学分析的结果，lncRNA USP30-AS1 在 AML 中高表达，USP30-AS1 的高表达和 USP30-AS1 基因启动子 Cg03124318 位点的低甲基化水平均与 AML 的不良预后相关。本研究通过敲低和过表达 USP30-AS1 来确定其在 AML 细胞系中的作用。通过高通量测序来探索受 USP30-AS1 调控的基因。结果表明，USP30-AS1 促进 AML 细胞的活力并抑制细胞凋亡。受 USP30-AS1 调控的基因主要与遗传调控和免疫系统有关。其中，USP30 和 ANKRD13A 基因在染色体上与 USP30-AS1 基因临近。敲低 USP30，但不敲低 ANKRD13A，可消除 USP30-AS1 的促癌作用。ANKRD13A 识别 HLA-I 上的 Lys-63 连接的多泛素链。USP30-AS1 通过上调 ANKRD13A 诱导 HLA-I 从细胞膜内化，这可能诱导 AML 细胞的免疫逃逸。ChIP 分析显示，USP30-AS1 对 USP30 和 ANKRD13A 的调控作用与 H3K4me3 和 H3K27Ac 有关。总之，USP30-AS1 可能通过顺式调控 USP30 和 ANKRD13A 促进 AML 细胞的存活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/3049470c20b4/13577_2021_636_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/b58ad297f34a/13577_2021_636_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/6c65b55a76ff/13577_2021_636_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/027d2f6fa6cb/13577_2021_636_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/d3ebc21b5df2/13577_2021_636_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/6a68dec59896/13577_2021_636_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/f9b4b82eaa43/13577_2021_636_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/cc10a6051b88/13577_2021_636_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/3049470c20b4/13577_2021_636_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/b58ad297f34a/13577_2021_636_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/6c65b55a76ff/13577_2021_636_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/027d2f6fa6cb/13577_2021_636_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/d3ebc21b5df2/13577_2021_636_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/6a68dec59896/13577_2021_636_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/f9b4b82eaa43/13577_2021_636_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/cc10a6051b88/13577_2021_636_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/50d4/8732929/3049470c20b4/13577_2021_636_Fig8_HTML.jpg

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