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N -甲基腺苷 RNA 去甲基酶 FTO 调控细胞外基质相关基因并促进胰腺癌细胞迁移和侵袭。

N -methyladenosine RNA demethylase FTO regulates extracellular matrix-related genes and promotes pancreatic cancer cell migration and invasion.

机构信息

Department of Hepatobiliary Surgery in East Hospital, Renmin Hospital of Wuhan University, Wuhan, China.

The State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education, School & Hospital of Stomatology, Wuhan University, Wuhan, China.

出版信息

Cancer Med. 2023 Feb;12(3):3731-3743. doi: 10.1002/cam4.5054. Epub 2022 Jul 25.

DOI:10.1002/cam4.5054
PMID:35879877
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9939218/
Abstract

Pancreatic cancer (PC) is a deadly disease, and its post-transcriptional gene regulation mechanism remains unclear. The abundant extracellular matrix (ECM) in PC plays an important role in tumor progression. This study is the first to focus on the role of N -methyladenosine (m A) RNA methylation, an emerging post-transcriptional regulatory mechanism, in the regulation of the ECM in PC. Here, we found that ADAMTS2, COL12A1, and THBS2 were associated with the prognosis of PC by comprehensive analysis of differentially expressed genes from two independent GEO expression profile datasets and m A-related genes in RMVar database (PAAD). GO and KEGG enrichment analysis found that these m A-related targets are chiefly functionally concentrated in the ECM region and participate in ECM signal transduction. Correlation analysis revealed that these genes can be regulated by the demethylase FTO. Cell biology function assays showed that knockdown of FTO-inhibited PC cell abilities to migrate and invade in vitro. qRT-PCR and MeRIP experiments showed that after knockdown of FTO, the mRNA levels of ADAMTS2, COL12A1, and THBS2 and their m A modification levels were significantly reduced. These results indicate that m A RNA demethylation is associated with the regulation of ECM in PC. In conclusion, m A RNA demethylase FTO regulates ECM-related genes and promotes PC cell abilities to migrate and invade, our work provides a new perspective on the molecular mechanism of PC progression.

摘要

胰腺癌（PC）是一种致命的疾病，其转录后基因调控机制尚不清楚。PC 中丰富的细胞外基质（ECM）在肿瘤进展中起着重要作用。本研究首次关注 N -甲基腺苷（m A）RNA 甲基化这一新兴的转录后调控机制在 PC 中 ECM 调控中的作用。在这里，我们通过综合分析两个独立的 GEO 表达谱数据集和 RMVar 数据库中的 m A 相关基因，发现 ADAMTS2、COL12A1 和 THBS2 与 PC 的预后相关。GO 和 KEGG 富集分析发现，这些 m A 相关靶标主要集中在 ECM 区域，并参与 ECM 信号转导。相关性分析表明，这些基因可以被去甲基酶 FTO 调节。细胞生物学功能测定表明，敲低 FTO 可抑制 PC 细胞体外迁移和侵袭的能力。qRT-PCR 和 MeRIP 实验表明，敲低 FTO 后，ADAMTS2、COL12A1 和 THBS2 的 mRNA 水平及其 m A 修饰水平显著降低。这些结果表明 m A RNA 去甲基化与 PC 中 ECM 的调节有关。总之，m A RNA 去甲基酶 FTO 调节 ECM 相关基因并促进 PC 细胞迁移和侵袭的能力，我们的工作为 PC 进展的分子机制提供了新的视角。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/1fefe38cea14/CAM4-12-3731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/aabf9ba14314/CAM4-12-3731-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/7441226a5e12/CAM4-12-3731-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/6fec018ff42f/CAM4-12-3731-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/5067b499a1db/CAM4-12-3731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/625e4787fced/CAM4-12-3731-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/596cee165701/CAM4-12-3731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/1fefe38cea14/CAM4-12-3731-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/aabf9ba14314/CAM4-12-3731-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/7441226a5e12/CAM4-12-3731-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/6fec018ff42f/CAM4-12-3731-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/5067b499a1db/CAM4-12-3731-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/625e4787fced/CAM4-12-3731-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/596cee165701/CAM4-12-3731-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/738b/9939218/1fefe38cea14/CAM4-12-3731-g001.jpg

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