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毫安读数器YTHDF3通过调节CENPI的稳定性促进三阴性乳腺癌进展。

The mA reader YTHDF3 promotes TNBC progression by regulating CENPI stabilization.

作者信息

Zhang Yulu, Chen Shunji, Wu Qiaosheng

机构信息

Department of Breast Surgery, Third Hospital of Nanchang, Nanchang, Jiangxi, China.

Department of Orthopedics, Third Hospital of Nanchang, Nanchang, Jiangxi, China.

出版信息

Front Oncol. 2025 May 8;15:1546723. doi: 10.3389/fonc.2025.1546723. eCollection 2025.

DOI:10.3389/fonc.2025.1546723
PMID:40406242
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12095154/
Abstract

BACKGROUND: RNA -methyladenosine (mA) readers mediate cancer progression. However, the role of eiptranscriptomic modifications such as mA in the regulation of TNBC progression is unclear. METHODS: High-throughput library screening identifies the key mA regulator YTHDF3 in TNBC. Cell and animal experiments were used to identify that YTHDF3 promoted TNBC tumorigenesis to enhance Centromere protein I (CENPI) translation via mA modification. RESULTS: We showed that the -methyladenosine (mA) reader YTHDF3 was an independent risk factor in TNBC and was associated with poor prognosis of patients. Notedly, overexpression YTHDF3 promoted TNBC tumorigenesis in an mA modification, while TNBC knockdown markedly inhibited proliferation and migratory ability of tumor cells and in vivo. Mechanistically, Mechanistically, YTHDF3 interacted with Centromere protein I (CENPI) mRNAs to prolong stability of mA-modified RNA. CONCLUSION: Our findings indicated that mA reader YTHDF3 contributed to tumorigenesis and poor prognosis, providing a potential prognostic biomarker and therapeutic target for TNBC.

摘要

背景：RNA甲基腺苷（mA）阅读蛋白介导癌症进展。然而，诸如mA等表观转录组修饰在三阴性乳腺癌（TNBC）进展调控中的作用尚不清楚。 方法：高通量文库筛选确定了TNBC中的关键mA调节因子YTHDF3。利用细胞和动物实验确定YTHDF3通过mA修饰促进TNBC肿瘤发生以增强着丝粒蛋白I（CENPI）的翻译。 结果：我们发现，甲基腺苷（mA）阅读蛋白YTHDF3是TNBC的一个独立危险因素，与患者预后不良相关。值得注意的是，YTHDF3的过表达通过mA修饰促进TNBC肿瘤发生，而TNBC的敲低显著抑制肿瘤细胞在体内外的增殖和迁移能力。机制上，YTHDF3与着丝粒蛋白I（CENPI）mRNA相互作用以延长mA修饰RNA的稳定性。 结论：我们的研究结果表明，mA阅读蛋白YTHDF3促进肿瘤发生并导致预后不良，为TNBC提供了一个潜在的预后生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/9ef7d0bd4830/fonc-15-1546723-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/f275ccd2a119/fonc-15-1546723-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/54527d23303b/fonc-15-1546723-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/786ca218f933/fonc-15-1546723-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/3f1db91efb8e/fonc-15-1546723-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/664fa8f1c542/fonc-15-1546723-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/9ef7d0bd4830/fonc-15-1546723-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/f275ccd2a119/fonc-15-1546723-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/54527d23303b/fonc-15-1546723-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/786ca218f933/fonc-15-1546723-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/3f1db91efb8e/fonc-15-1546723-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/664fa8f1c542/fonc-15-1546723-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1c87/12095154/9ef7d0bd4830/fonc-15-1546723-g006.jpg

相似文献

[1]
The mA reader YTHDF3 promotes TNBC progression by regulating CENPI stabilization.

Front Oncol. 2025-5-8

[2]
The human 18S rRNA m6A methyltransferase METTL5 promotes tumorigenesis via DEPDC1 in lung squamous cell carcinoma.

Front Oncol. 2025-2-13

[3]
m A reader YTHDF3 triggers the progression of hepatocellular carcinoma through the YTHDF3/m A-EGFR/STAT3 axis and EMT.

Mol Carcinog. 2023-10

[4]
N-methyladenosine reader YTHDF3 contributes to the aerobic glycolysis of osteosarcoma through stabilizing PGK1 stability.

J Cancer Res Clin Oncol. 2023-7

[5]
YTHDF3 facilitates triple-negative breast cancer progression and metastasis by stabilizing ZEB1 mRNA in an mA-dependent manner.

Ann Transl Med. 2022-1

[6]
A functional loop between YTH domain family protein YTHDF3 mediated mA modification and phosphofructokinase PFKL in glycolysis of hepatocellular carcinoma.

J Exp Clin Cancer Res. 2022-12-6

[7]
Long noncoding RNA GAS5 inhibits progression of colorectal cancer by interacting with and triggering YAP phosphorylation and degradation and is negatively regulated by the mA reader YTHDF3.

Mol Cancer. 2019-10-16

[8]
Autophagy induction promoted by mA reader YTHDF3 through translation upregulation of FOXO3 mRNA.

Nat Commun. 2022-10-4

[9]
YTHDF3 modulates the progression of breast cancer cells by regulating FGF2 through mA methylation.

Front Cell Dev Biol. 2024-9-20

[10]
The m6A readers and aberrations associated with metastasis and predict poor prognosis in breast cancer patients.

Am J Cancer Res. 2020-8-1

本文引用的文献

[1]
METTL14 suppresses the expression of YAP1 and the stemness of triple-negative breast cancer.

J Exp Clin Cancer Res. 2024-11-20

[2]
N-Methyladenosine Regulates Cilia Elongation in Cancer Cells by Modulating HDAC6 Expression.

Adv Sci (Weinh). 2025-1

[3]
Immune infiltration related CENPI associates with the malignant features and drug resistance of lung adenocarcinoma.

Biochim Biophys Acta Mol Basis Dis. 2024-3

[4]
MA demethylase ALKBH5 regulates FOXO1 mRNA stability and chemoresistance in triple-negative breast cancer.

Redox Biol. 2024-2

[5]
A positive feedback circuit driven by mA-modified circular RNA facilitates colorectal cancer liver metastasis.

Mol Cancer. 2023-12-13

[6]
Pan-Cancer Analysis Reveals CENPI as a Potential Biomarker and Therapeutic Target in Adrenocortical Carcinoma.

J Inflamm Res. 2023-7-12

[7]
Epigenetic modification of mA regulator proteins in cancer.

Mol Cancer. 2023-6-30

[8]
Targeting mA binding protein YTHDFs for cancer therapy.

Bioorg Med Chem. 2023-7-15

[9]
N6-methyladenosine reader YTHDF family in biological processes: Structures, roles, and mechanisms.

Front Immunol. 2023

[10]
A functional loop between YTH domain family protein YTHDF3 mediated mA modification and phosphofructokinase PFKL in glycolysis of hepatocellular carcinoma.

J Exp Clin Cancer Res. 2022-12-6

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