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关于在宫颈鳞癌中 mA 修饰与非编码 RNA 相互作用的新见解。

New insights on the interaction between mA modification and non-coding RNA in cervical squamous cell carcinoma.

机构信息

The Second Department of Gynecology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, 830011, China.

Xinjiang Key Laboratory of Oncology, Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, 830011, China.

出版信息

World J Surg Oncol. 2023 Jan 30;21(1):25. doi: 10.1186/s12957-023-02907-z.

DOI:10.1186/s12957-023-02907-z
PMID:36710350
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9885588/
Abstract

BACKGROUND

N-Methyladenosine (mA) and long non-coding RNAs (lncRNAs) are both crucial regulators in human cancer growth and metastasis. However, their regulation on cervical squamous cell carcinoma (CSCC) is largely unclear. The present study aimed to explore the role of mA-associated lncRNAs in CSCC.

METHODS

We screened the expression of methylation modification-related enzymes in CECC samples from TCGA. The qRT-PCR was used to detect METTL3 and lncRNA METTL4-2 expression. The biological activities of METTL3 in CSCC cells were evaluated by CCK-8, colony formation, transwell, wound healing, and xenograft tumor assays, respectively. The SRAMP tool was used to screen mA modification sites of METTL4-2. Finally, the quantitative analysis of mA modification was carried out by MeRIP.

RESULTS

METTL3 expression was upregulated in CSCC cells and tissues. Biological function and function loss analysis indicated that METTL3 promoted the migration and proliferation of CSCC cells. In addition, METTL3 promoted CSCC tumor growth in vivo. Mechanically, METTL3 installed the mA modification and enhanced METTL4-2 transcript stability to increase its expression. Meanwhile, the mA "reader" YTHDF1 recognized METTL4-2 installed by METTL3 and facilitated the translation of METTL4-2.

CONCLUSIONS

In conclusion, our study highlights the function and mechanism of METTL3-induced METTL4-2 in CSCC. These findings support that METTL3-stabilized METTL4-2 promoted CSCC progression via a mA-dependent modality, which provides new insights into therapeutic strategies for CSCC.

摘要

背景

N6-甲基腺苷（m6A）和长链非编码 RNA（lncRNA）都是人类癌症生长和转移的关键调节因子。然而，它们对宫颈鳞状细胞癌（CSCC）的调节作用在很大程度上尚不清楚。本研究旨在探讨 m6A 相关 lncRNA 在 CSCC 中的作用。

方法

我们从 TCGA 中筛选 CSCC 样本中甲基化修饰相关酶的表达。qRT-PCR 用于检测 METTL3 和 lncRNA METTL4-2 的表达。分别通过 CCK-8、集落形成、transwell、划痕愈合和异种移植肿瘤实验评估 METTL3 在 CSCC 细胞中的生物学活性。SRAMP 工具用于筛选 METTL4-2 的 m6A 修饰位点。最后，通过 MeRIP 进行 m6A 修饰的定量分析。

结果

METTL3 在 CSCC 细胞和组织中表达上调。生物学功能和功能丧失分析表明，METTL3 促进了 CSCC 细胞的迁移和增殖。此外，METTL3 促进了 CSCC 肿瘤在体内的生长。在机制上，METTL3 安装了 m6A 修饰并增强了 METTL4-2 转录本的稳定性，从而增加了其表达。同时，m6A“阅读器”YTHDF1 识别由 METTL3 安装的 METTL4-2，并促进了 METTL4-2 的翻译。

结论

总之，本研究强调了 METTL3 诱导的 METTL4-2 在 CSCC 中的功能和机制。这些发现支持 METTL3 稳定的 METTL4-2 通过 m6A 依赖的方式促进 CSCC 进展，为 CSCC 的治疗策略提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/6180e9e0b9ff/12957_2023_2907_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/fd301ad94c9f/12957_2023_2907_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/4302f73696a0/12957_2023_2907_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/26f7a86083ae/12957_2023_2907_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/e431b163394e/12957_2023_2907_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/b3b3c66f3395/12957_2023_2907_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/6180e9e0b9ff/12957_2023_2907_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/fd301ad94c9f/12957_2023_2907_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/4302f73696a0/12957_2023_2907_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/26f7a86083ae/12957_2023_2907_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/e431b163394e/12957_2023_2907_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/b3b3c66f3395/12957_2023_2907_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b96c/9885588/6180e9e0b9ff/12957_2023_2907_Fig6_HTML.jpg

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