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长链非编码 RNA OIP5-AS1 通过调节食管癌细胞中的 GPX4 促进铁死亡和免疫逃逸。

LncRNA OIP5-AS1 Knockdown Facilitated the Ferroptosis and Immune Evasion by Modulating the GPX4 in Oesophageal Carcinoma.

机构信息

Department of Gastroenterology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, China.

Department of Pathology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, 200233, China.

出版信息

Comput Math Methods Med. 2022 Jul 15;2022:8103198. doi: 10.1155/2022/8103198. eCollection 2022.

DOI:10.1155/2022/8103198
PMID:35872956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9307385/
Abstract

OBJECTIVE

Oesophageal cancer (EC) is an extremely invasive malignancy, which has bad prognosis that requires safe and effective treatment modalities. Immunotherapy has provided new ideas for the treatment of EC in recent years. This project was conducted to probe into the role and mechanism of lncRNA OIP5-AS1 in ferroptosis and immunotherapy of EC.

METHODS

Cell viability and multiplication were assessed through CCK-8, colony formation assays. Levels of Fe, MDA, and lipid ROS were applied to determine ferroptosis. GPX4 and OIP5-AS1 levels were examined through real-time PCR assay. The relationship between OIP5-AS1 and GPX4 was estimated through RNA immunoprecipitation assay. Flow cytometry was applied to examine the effect of OIP5-AS1 on CD8+ T cells.

RESULTS

OIP5-AS1 inhibition significantly inhibited EC cell viability and proliferation, induced ferroptosis, and downregulated GPX4 levels, while GPX4 reversed these effects. OIP5-AS1/GPX4 induced CD8+ T cell interaction and induced apoptosis through PD-1/PD-L1 immune checkpoints of CD8+ T cells.

CONCLUSION

OIP5-AS1/GPX4 promotes EC development and relieved ferroptosis; furthermore, OIP5-AS1/GPX4 facilitated immune evasion via modulation of PD-1/PD-L1, suggesting aiming at OIP5-AS1 is a possible route which might enhance the effectiveness of immunotherapy.

摘要

目的

食管癌（EC）是一种极具侵袭性的恶性肿瘤，预后不良，需要安全有效的治疗方法。近年来，免疫疗法为 EC 的治疗提供了新的思路。本项目旨在探讨 lncRNA OIP5-AS1 在 EC 中的铁死亡和免疫治疗中的作用和机制。

方法

通过 CCK-8、集落形成实验评估细胞活力和增殖。应用铁、MDA 和脂质 ROS 水平来确定铁死亡。通过实时 PCR 检测 GPX4 和 OIP5-AS1 水平。通过 RNA 免疫沉淀测定评估 OIP5-AS1 和 GPX4 之间的关系。通过流式细胞术评估 OIP5-AS1 对 CD8+T 细胞的影响。

结果

OIP5-AS1 抑制显著抑制 EC 细胞活力和增殖，诱导铁死亡，并下调 GPX4 水平，而 GPX4 逆转了这些作用。OIP5-AS1/GPX4 通过 CD8+T 细胞的 PD-1/PD-L1 免疫检查点诱导 CD8+T 细胞相互作用并诱导细胞凋亡。

结论

OIP5-AS1/GPX4 促进 EC 的发展并缓解铁死亡；此外，OIP5-AS1/GPX4 通过调节 PD-1/PD-L1 促进免疫逃逸，表明针对 OIP5-AS1 可能是增强免疫治疗效果的一种途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/be594d6ea9de/CMMM2022-8103198.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/7dbafc661025/CMMM2022-8103198.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/50456e9d46ff/CMMM2022-8103198.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/05d134ea9530/CMMM2022-8103198.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/adbb2e3644c8/CMMM2022-8103198.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/be594d6ea9de/CMMM2022-8103198.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/7dbafc661025/CMMM2022-8103198.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/50456e9d46ff/CMMM2022-8103198.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/05d134ea9530/CMMM2022-8103198.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/adbb2e3644c8/CMMM2022-8103198.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ff1c/9307385/be594d6ea9de/CMMM2022-8103198.005.jpg

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