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与miRNA-基因相互作用结果相关的肿瘤突变负担介导了肝细胞癌患者的生存。

Tumor mutation burden associated with miRNA-gene interaction outcome mediates the survival of patients with liver hepatocellular carcinoma.

作者信息

Yu Qing-Jiang, Liang Yi-Zhi, Mei Xiao-Ping, Fang Tai-Yong

机构信息

Department of Hepatobiliary Surgery, First Affiliated Hospital of Jiaxing University, Jiaxing 314000, China.

Department of Gastroenterology, Second Affiliated Hospital, Fujian Medical University, Quanzhou 362000, China.

出版信息

EXCLI J. 2020 Jun 22;19:861-871. doi: 10.17179/excli2020-1224. eCollection 2020.

DOI:10.17179/excli2020-1224
PMID:32665773
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7355149/
Abstract

Tumor mutation burden (TMB) is associated with immunogenic responses and the survival of cancer patients. This study demonstrates how TMB levels impact the immune-related cells, genes, and miRNAs, and how miRNA/gene interactions respond to variations in the survival rate of patients with liver hepatocellular carcinoma (LIHC). LIHC patients were divided into two groups, either a low TMB (< median) or a high TMB (≥ median) group. We found that high TMB plays a positive role in immune-mediated infiltration, generating more CD4 T-cells and memory B cells. Among the 21 immune genes that altered significantly, only and were expected to up-regulate in LIHC patients with high TMB. A total of 19 miRNAs, which regulate various functional pathways, were significantly altered in patients with LIHC. One of the miRNA/gene pair, hsa-miR-33a/ was significantly associated with the survival rate of LIHC patients. Our results suggest that LIHC patients with high TMB can be treated more effectively with immunotherapy.

摘要

肿瘤突变负荷（TMB）与免疫原性反应及癌症患者的生存相关。本研究展示了TMB水平如何影响免疫相关细胞、基因和微小RNA（miRNA），以及miRNA/基因相互作用如何响应肝细胞癌（LIHC）患者生存率的变化。LIHC患者被分为两组，即低TMB（<中位数）组或高TMB（≥中位数）组。我们发现高TMB在免疫介导的浸润中起积极作用，产生更多的CD4 T细胞和记忆B细胞。在显著改变的21个免疫基因中，只有 和 预计在高TMB的LIHC患者中上调。共有19个调控各种功能途径的miRNA在LIHC患者中显著改变。其中一对miRNA/基因，即hsa-miR-33a/ 与LIHC患者的生存率显著相关。我们的结果表明，高TMB的LIHC患者可能通过免疫疗法得到更有效的治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/4927dcc0be80/EXCLI-19-861-g-006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/f3268787e9ed/EXCLI-19-861-g-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/874165dfc3ce/EXCLI-19-861-g-002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/54db2ba43e30/EXCLI-19-861-g-003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/6bf287f72b74/EXCLI-19-861-g-004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/44e11bcc55fe/EXCLI-19-861-g-005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/4927dcc0be80/EXCLI-19-861-g-006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/f3268787e9ed/EXCLI-19-861-g-001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/874165dfc3ce/EXCLI-19-861-g-002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/54db2ba43e30/EXCLI-19-861-g-003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/6bf287f72b74/EXCLI-19-861-g-004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/44e11bcc55fe/EXCLI-19-861-g-005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/77a7/7355149/4927dcc0be80/EXCLI-19-861-g-006.jpg

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PNMA1, regulated by miR-33a-5p, promotes proliferation and EMT in hepatocellular carcinoma by activating the Wnt/β-catenin pathway.PNMA1 通过激活 Wnt/β-catenin 通路促进肝癌的增殖和 EMT，受 miR-33a-5p 的调控。
Biomed Pharmacother. 2018 Dec;108:492-499. doi: 10.1016/j.biopha.2018.09.059. Epub 2018 Sep 19.
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Global cancer statistics 2018: GLOBOCAN estimates of incidence and mortality worldwide for 36 cancers in 185 countries.
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CA Cancer J Clin. 2018 Nov;68(6):394-424. doi: 10.3322/caac.21492. Epub 2018 Sep 12.
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ADAP1 limits neonatal cardiomyocyte hypertrophy by reducing integrin cell surface expression.ADAP1 通过减少整合素细胞表面表达来限制新生儿心肌细胞肥大。
Sci Rep. 2018 Sep 11;8(1):13605. doi: 10.1038/s41598-018-31784-w.
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Nivolumab plus Ipilimumab in Lung Cancer with a High Tumor Mutational Burden.纳武利尤单抗联合伊匹单抗治疗高肿瘤突变负荷肺癌。
N Engl J Med. 2018 May 31;378(22):2093-2104. doi: 10.1056/NEJMoa1801946. Epub 2018 Apr 16.
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