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m6A 甲基化 KCTD21-AS1 通过 CD47 和细胞自噬通过 TIPR 调节巨噬细胞吞噬作用。

m6A-methylated KCTD21-AS1 regulates macrophage phagocytosis through CD47 and cell autophagy through TIPR.

机构信息

Department of Biochemistry and Molecular Biology, Binzhou Medical University, YanTai, Shandong, 264003, PR China.

Shandong Laboratory of Advanced Materials and Green Manufacturing (Yantai), Shandong, 264000, PR China.

出版信息

Commun Biol. 2024 Feb 21;7(1):215. doi: 10.1038/s42003-024-05854-x.

DOI:10.1038/s42003-024-05854-x
PMID:38383737
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10881998/
Abstract

Blocking immune checkpoint CD47/SIRPα is a useful strategy to engineer macrophages for cancer immunotherapy. However, the roles of CD47-related noncoding RNA in regulating macrophage phagocytosis for lung cancer therapy remain unclear. This study aims to investigate the effects of long noncoding RNA (lncRNA) on the phagocytosis of macrophage via CD47 and the proliferation of non-small cell lung cancer (NSCLC) via TIPRL. Our results demonstrate that lncRNA KCTD21-AS1 increases in NSCLC tissues and is associated with poor survival of patients. KCTD21-AS1 and its m6A modification by Mettl14 promote NSCLC cell proliferation. miR-519d-5p gain suppresses the proliferation and metastasis of NSCLC cells by regulating CD47 and TIPRL. Through ceRNA with miR-519d-5p, KCTD21-AS1 regulates the expression of CD47 and TIPRL, which further regulates macrophage phagocytosis and cancer cell autophagy. Low miR-519d-5p in patients with NSCLC corresponds with poor survival. High TIPRL or CD47 levels in patients with NSCLC corresponds with poor survival. In conclusion, we demonstrate that KCTD21-AS1 and its m6A modification promote NSCLC cell proliferation, whereas miR-519d-5p inhibits this process by regulating CD47 and TIPRL expression, which further affects macrophage phagocytosis and cell autophagy. This study provides a strategy through miR-519-5p gain or KCTD21-AS1 depletion for NSCLC therapy by regulating CD47 and TIPRL.

摘要

阻断免疫检查点 CD47/SIRPα 是一种将巨噬细胞工程化为癌症免疫疗法的有效策略。然而，CD47 相关非编码 RNA 在调节肺癌治疗中巨噬细胞吞噬作用的作用仍不清楚。本研究旨在探讨长链非编码 RNA（lncRNA）通过 CD47 调节巨噬细胞吞噬作用和通过 TIPRL 调节非小细胞肺癌（NSCLC）增殖的作用。我们的结果表明，lncRNA KCTD21-AS1 在 NSCLC 组织中增加，并与患者的不良生存相关。KCTD21-AS1 及其由 Mettl14 进行的 m6A 修饰促进 NSCLC 细胞增殖。miR-519d-5p 的获得通过调节 CD47 和 TIPRL 抑制 NSCLC 细胞的增殖和转移。通过与 miR-519d-5p 的 ceRNA，KCTD21-AS1 调节 CD47 和 TIPRL 的表达，进而调节巨噬细胞吞噬作用和癌细胞自噬。NSCLC 患者中 miR-519d-5p 水平低与生存不良相关。NSCLC 患者中 TIPRL 或 CD47 水平高与生存不良相关。总之，我们证明 KCTD21-AS1 及其 m6A 修饰促进 NSCLC 细胞增殖，而 miR-519d-5p 通过调节 CD47 和 TIPRL 的表达抑制这一过程，从而进一步影响巨噬细胞吞噬作用和细胞自噬。本研究通过 miR-519d-5p 的获得或 KCTD21-AS1 的耗竭提供了一种通过调节 CD47 和 TIPRL 治疗 NSCLC 的策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/ee773f627dec/42003_2024_5854_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/25d22e919f51/42003_2024_5854_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/94c760e122e5/42003_2024_5854_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/3955cebbf178/42003_2024_5854_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/3575fc42f02a/42003_2024_5854_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/163f4c03d5bc/42003_2024_5854_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/6733b59e7104/42003_2024_5854_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/dfdb883bf639/42003_2024_5854_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/ee773f627dec/42003_2024_5854_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/25d22e919f51/42003_2024_5854_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/94c760e122e5/42003_2024_5854_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/3955cebbf178/42003_2024_5854_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/3575fc42f02a/42003_2024_5854_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/163f4c03d5bc/42003_2024_5854_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/6733b59e7104/42003_2024_5854_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/dfdb883bf639/42003_2024_5854_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c8a/10881998/ee773f627dec/42003_2024_5854_Fig8_HTML.jpg

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引用本文的文献

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[3]
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[4]
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Front Oncol. 2025-7-16

[5]
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[6]
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J Transl Med. 2025-6-2

[7]
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[8]
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本文引用的文献

[1]
WFDC21P promotes triple-negative breast cancer proliferation and migration through WFDC21P/miR-628/SMAD3 axis.

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