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非编码 RNA 作为癌症免疫治疗的新兴耐药机制:基础证据与治疗意义。

Noncoding RNAs as an emerging resistance mechanism to immunotherapies in cancer: basic evidence and therapeutic implications.

机构信息

Institute for Translational Medicine, The Affiliated Hospital of Qingdao University, College of Medicine, Qingdao University, Qingdao, China.

出版信息

Front Immunol. 2023 Sep 12;14:1268745. doi: 10.3389/fimmu.2023.1268745. eCollection 2023.


DOI:10.3389/fimmu.2023.1268745
PMID:37767098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10520974/
Abstract

The increasing knowledge in the field of oncoimmunology has led to extensive research into tumor immune landscape and a plethora of clinical immunotherapy trials in cancer patients. Immunotherapy has become a clinically beneficial alternative to traditional treatments by enhancing the power of the host immune system against cancer. However, it only works for a minority of cancers. Drug resistance continues to be a major obstacle to the success of immunotherapy in cancer. A fundamental understanding of the detailed mechanisms underlying immunotherapy resistance in cancer patients will provide new potential directions for further investigations of cancer treatment. Noncoding RNAs (ncRNAs) are tightly linked with cancer initiation and development due to their critical roles in gene expression and epigenetic modulation. The clear appreciation of the role of ncRNAs in tumor immunity has opened new frontiers in cancer research and therapy. Furthermore, ncRNAs are increasingly acknowledged as a key factor influencing immunotherapeutic treatment outcomes. Here, we review the available evidence on the roles of ncRNAs in immunotherapy resistance, with an emphasis on the associated mechanisms behind ncRNA-mediated immune resistance. The clinical implications of immune-related ncRNAs are also discussed, shedding light on the potential ncRNA-based therapies to overcome the resistance to immunotherapy.

摘要

肿瘤免疫学领域知识的不断增加,促使人们对肿瘤免疫景观进行了广泛的研究,并在癌症患者中开展了大量的临床免疫治疗试验。免疫疗法通过增强宿主免疫系统对癌症的作用,已成为传统治疗的一种有临床益处的替代方法。然而,它仅适用于少数癌症。耐药性仍然是免疫疗法在癌症中取得成功的主要障碍。深入了解癌症患者免疫治疗耐药的详细机制,将为癌症治疗的进一步研究提供新的潜在方向。

非编码 RNA(ncRNA)由于在基因表达和表观遗传调控中的关键作用,与癌症的发生和发展密切相关。ncRNA 在肿瘤免疫中的作用的明确认识为癌症研究和治疗开辟了新的前沿。此外,ncRNA 被越来越多地认为是影响免疫治疗治疗效果的关键因素。

在这里,我们回顾了 ncRNA 在免疫治疗耐药性中的作用的现有证据,重点讨论了 ncRNA 介导的免疫耐药性背后的相关机制。还讨论了免疫相关 ncRNA 的临床意义,为克服免疫治疗耐药性提供了基于 ncRNA 的治疗方法的潜在思路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/1aebd1eda197/fimmu-14-1268745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/5257e44f3a61/fimmu-14-1268745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/858224131721/fimmu-14-1268745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/88f37d019390/fimmu-14-1268745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/e128be248691/fimmu-14-1268745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/23b53cc7a426/fimmu-14-1268745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/2b3e1c820dd9/fimmu-14-1268745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/1aebd1eda197/fimmu-14-1268745-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/5257e44f3a61/fimmu-14-1268745-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/858224131721/fimmu-14-1268745-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/88f37d019390/fimmu-14-1268745-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/e128be248691/fimmu-14-1268745-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/23b53cc7a426/fimmu-14-1268745-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/2b3e1c820dd9/fimmu-14-1268745-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf85/10520974/1aebd1eda197/fimmu-14-1268745-g007.jpg

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Noncoding RNAs as an emerging resistance mechanism to immunotherapies in cancer: basic evidence and therapeutic implications.

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[5]
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引用本文的文献

[1]
Multiplex imaging analysis of the tumor immune microenvironment for guiding precision immunotherapy.

Front Immunol. 2025-7-11

[2]
Acute PM2.5 Exposure in Distinct NSCLC Cell Lines Reveals Strong Oxidative Stress and Therapy Resistance Signatures Through Transcriptomic Analysis.

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[3]
Immune checkpoints and ncRNAs: pioneering immunotherapy approaches for hematological malignancies.

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[4]
Synergistic Immunoregulation: harnessing CircRNAs and PiRNAs to Amplify PD-1/PD-L1 Inhibition Therapy.

Int J Nanomedicine. 2024

[5]
The important regulatory roles of circRNA‑encoded proteins or peptides in cancer pathogenesis (Review).

Int J Oncol. 2024-2

本文引用的文献

[1]
Identification of cuproptosis-related lncRNA for predicting prognosis and immunotherapeutic response in cervical cancer.

Sci Rep. 2023-7-3

[2]
Non-coding RNA-mediated modulation of ferroptosis in cardiovascular diseases.

Biomed Pharmacother. 2023-8

[3]
Oncogenic miR-93-5p/Gal-9 axis drives CD8 (+) T-cell inactivation and is a therapeutic target for hepatocellular carcinoma immunotherapy.

Cancer Lett. 2023-6-28

[4]
Non-coding RNAs regulating mitochondrial function in cardiovascular diseases.

J Mol Med (Berl). 2023-5

[5]
Sialic acid-targeted cyclodextrin-based nanoparticles deliver CSF-1R siRNA and reprogram tumour-associated macrophages for immunotherapy of prostate cancer.

Eur J Pharm Sci. 2023-6-1

[6]
Exosome-derived circCCAR1 promotes CD8 + T-cell dysfunction and anti-PD1 resistance in hepatocellular carcinoma.

Mol Cancer. 2023-3-18

[7]
Tumor-associated nonmyelinating Schwann cell-expressed promotes pancreatic cancer kynurenine pathway and tumor immune exclusion.

Sci Adv. 2023-2-3

[8]
Overcoming the resistance of hepatocellular carcinoma to PD-1/PD-L1 inhibitor and the resultant immunosuppression by CD38 siRNA-loaded extracellular vesicles.

Oncoimmunology. 2023

[9]
Identification and validation of a ferroptosis-related lncRNA signature to robustly predict the prognosis, immune microenvironment, and immunotherapy efficiency in patients with clear cell renal cell carcinoma.

PeerJ. 2022

[10]
Circ_0000052/miR-382-3p axis induces PD-L1 expression and regulates cell proliferation and immune evasion in head and neck squamous cell carcinoma.

J Cell Mol Med. 2023-1

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