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长非编码 RNA MAGEA4-AS1 与 p53 结合增强 MK2 信号通路并促进口腔鳞状细胞癌的增殖和转移。

Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma.

机构信息

Peking University Shenzhen Hospital Clinical College, The Fifth School of Clinical Medicine, Anhui Medical University, Hefei, Anhui, 230032, China.

Department of Oral and Maxillofacial Surgery, Stomatological Center, Peking University Shenzhen Hospital, Guangdong Provincial High-level Clinical Key Specialty, Guangdong Province Engineering Research Center of Oral Disease Diagnosis and Treatment, The Institute of Stomatology, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, Guangdong, 518036, China.

出版信息

Funct Integr Genomics. 2024 Sep 9;24(5):158. doi: 10.1007/s10142-024-01436-6.

DOI:10.1007/s10142-024-01436-6
PMID:39249547
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11384635/
Abstract

Long non-coding RNAs (lncRNAs) regulate the occurrence, development and progression of oral squamous cell carcinoma (OSCC). We elucidated the expression features of MAGEA4-AS1 in patients with OSCC and its activity as an OSCC biomarker. Furthermore, the impact of up-regulation of MAGEA4-AS1 on the cellular behaviors (proliferation, migration and invasion) of OSCC cells and intrinsic signal mechanisms were evaluated. Firstly, we analyzed MAGEA4-AS1 expression data in The Cancer Genome Atlas (TCGA) OSCC using a bioinformatics approach and in 45 pairs of OSCC tissues using qPCR. Then CCK-8, ethynyl deoxyuridine, colony formation, transwell and wound healing assays were conducted to assess changes in the cell proliferation, migration and invasion protential of shMAGEA4-AS1 HSC3 and CAL27 cells. The RNA sequence of MAGEA4-AS1 was identified using the rapid amplification of cDNA ends (RACE) assay. And whole-transcriptome sequencing was used to identify MAGEA4-AS1 affected genes. Additionally, dual-luciferase reporter system, RNA-binding protein immunoprecipitation (RIP), and rescue experiments were performed to clarify the role of the MAGEA4-AS1-p53-MK2 signaling pathway. As results, we found MAGEA4-AS1 was up-regulated in OSCC tissues. We identified a 418 nucleotides length of the MAGEA4-AS1 transcript and it primarily located in the cell nucleus. MAGEA4-AS1 stable knockdown weakened the proliferation, migration and invasion abilities of OSCC cells. Mechanistically, p53 protein was capable to activate MK2 gene transcription. RIP assay revealed an interaction between p53 and MAGEA4-AS1. MK2 up-regulation in MAGEA4-AS1 down-regulated OSCC cells restored MK2 and epithelial-to-mesenchymal transition related proteins' expression levels. In conclusion, MAGEA4-AS1-p53 complexes bind to MK2 promoter, enhancing the transcription of MK2 and activating the downstream signaling pathways, consequently promoting the proliferation and metastasis of OSCC cells. MAGEA4-AS1 may serve as a diagnostic marker and therapeutic target for OSCC patients.

摘要

长链非编码 RNA（lncRNA）调控口腔鳞状细胞癌（OSCC）的发生、发展和进展。我们阐明了 MAGEA4-AS1 在 OSCC 患者中的表达特征及其作为 OSCC 生物标志物的活性。此外，还评估了上调 MAGEA4-AS1 对 OSCC 细胞的细胞行为（增殖、迁移和侵袭）和内在信号机制的影响。首先，我们通过生物信息学方法分析了癌症基因组图谱（TCGA）OSCC 中的 MAGEA4-AS1 表达数据，并使用 qPCR 分析了 45 对 OSCC 组织中的 MAGEA4-AS1 表达数据。然后，通过 CCK-8、乙脒基脱氧尿苷、集落形成、Transwell 和划痕愈合实验评估了 shMAGEA4-AS1 HSC3 和 CAL27 细胞增殖、迁移和侵袭能力的变化。使用快速扩增 cDNA 末端（RACE）实验鉴定 MAGEA4-AS1 的 RNA 序列。并通过全转录组测序鉴定 MAGEA4-AS1 影响的基因。此外，还进行了双荧光素酶报告基因系统、RNA 结合蛋白免疫沉淀（RIP）和挽救实验，以阐明 MAGEA4-AS1-p53-MK2 信号通路的作用。结果发现，MAGEA4-AS1 在 OSCC 组织中上调。我们鉴定了 MAGEA4-AS1 转录本的 418 个核苷酸长度，它主要位于细胞核内。MAGEA4-AS1 稳定敲低削弱了 OSCC 细胞的增殖、迁移和侵袭能力。机制上，p53 蛋白能够激活 MK2 基因转录。RIP 实验显示 p53 和 MAGEA4-AS1 之间存在相互作用。在 MAGEA4-AS1 下调的 OSCC 细胞中上调 MK2 恢复了 MK2 和上皮-间充质转化相关蛋白的表达水平。总之，MAGEA4-AS1-p53 复合物结合到 MK2 启动子上，增强了 MK2 的转录，并激活了下游信号通路，从而促进了 OSCC 细胞的增殖和转移。MAGEA4-AS1 可作为 OSCC 患者的诊断标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/6585921f5969/10142_2024_1436_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/127023376328/10142_2024_1436_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/8ccaf63f68af/10142_2024_1436_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/09872da17f4e/10142_2024_1436_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/803fadbb21c5/10142_2024_1436_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/342c8d714399/10142_2024_1436_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/a6a98074506c/10142_2024_1436_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/6585921f5969/10142_2024_1436_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/127023376328/10142_2024_1436_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/8ccaf63f68af/10142_2024_1436_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/09872da17f4e/10142_2024_1436_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/803fadbb21c5/10142_2024_1436_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/342c8d714399/10142_2024_1436_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/a6a98074506c/10142_2024_1436_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4264/11384635/6585921f5969/10142_2024_1436_Fig7_HTML.jpg

相似文献

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Long non-coding RNA MAGEA4-AS1 binding to p53 enhances MK2 signaling pathway and promotes the proliferation and metastasis of oral squamous cell carcinoma.

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引用本文的文献

[1]
MK2 promotes p16 negative head and neck cancer migration, invasion, and metastasis.

Cancer Lett. 2025-7-10

[2]
TFAP2A-regulated CRNDE enhances colon cancer progression and chemoresistance via RIPK3 interaction.

Funct Integr Genomics. 2025-2-15

本文引用的文献

[1]
Structural basis for RAD18 regulation by MAGEA4 and its implications for RING ubiquitin ligase binding by MAGE family proteins.

EMBO J. 2024-4

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