RNA m6A修饰在乳腺癌中的研究进展

doi:10.3760/cma.j.cn371439-20241203-00090

国际肿瘤学杂志 ›› 2025, Vol. 52 ›› Issue (8): 532-537.doi: 10.3760/cma.j.cn371439-20241203-00090

RNA m⁶A修饰在乳腺癌中的研究进展

郭俊龙¹, 邹睿琪¹, 陈少强¹, 梁雨欣¹, 李菁², 雍苏南³, 何玉婷¹, 谢小兵¹, 李萍¹()

¹湖南中医药大学第一附属医院医学检验中心，长沙 410007
²湖南中医药大学第一附属医院肿瘤科，长沙 410007
³湖南中医药大学第一附属医院中医内科，长沙 410007

收稿日期:2024-12-03 修回日期:2025-01-24 出版日期:2025-08-08 发布日期:2025-09-15
通讯作者: 李萍 E-mail:lipingxt@163.com
基金资助:
湖南省自然科学基金(2025JJ90033);湖南省中医药管理局中医药科研计划(D2022112);湖南省临床医疗技术创新引导项目(2021SK51409);湖南省卫生健康委员会科研计划(202211004197)

Research progress of RNA m⁶A modification in breast cancer

Guo Junlong¹, Zou Ruiqi¹, Chen Shaoqiang¹, Liang Yuxin¹, Li Jing², Yong Sunan³, He Yuting¹, Xie Xiaobing¹, Li Ping¹()

¹Medical Laboratory Center， First Affiliated Hospital of Hunan University of Chinese Medicine， Changsha 410007， China
²Department of Oncology， First Affiliated Hospital of Hunan University of Chinese Medicine， Changsha 410007， China
³Department of Internal Medicine of Traditional Chinese Medicine， First Affiliated Hospital of Hunan University of Chinese Medicine， Changsha 410007， China

Received:2024-12-03 Revised:2025-01-24 Online:2025-08-08 Published:2025-09-15
Contact: Li Ping E-mail:lipingxt@163.com
Supported by:
Natural Science Foundation of Hunan Province of China(2025JJ90033);Traditional Chinese Medicine Research Program of the Administration of Traditional Chinese Medicine of Hunan Province(D2022112);Hunan Provincial Clinical Medical Technology Innovation Guidance Project(2021SK51409);Scientific Research Project of the Health Commission of Hunan Province(202211004197)

摘要/Abstract

摘要：

乳腺癌是全球女性常见的恶性肿瘤之一，其发病率呈逐年上升趋势，已成为重大公共健康问题。随着肿瘤生物学研究的不断深入，N⁶-甲基腺嘌呤（m⁶A）修饰作为一种重要的RNA修饰形式，越来越受到关注。m⁶A修饰是真核生物中最普遍的RNA修饰，广泛存在于几乎所有类型的RNA中，并在乳腺癌的发生、发展和转移过程中发挥关键作用。m⁶A修饰影响细胞的增殖、凋亡以及肿瘤微环境的变化，但其具体作用机制仍有待进一步深入研究。此外，m⁶A修饰的特定模式展现了其作为乳腺癌新型生物标志物的潜力，有望为早期诊断和预后评估提供新的研究方向。

关键词: 乳腺肿瘤, 表观基因组学, N⁶-甲基腺嘌呤

Abstract:

Breast cancer is one of the most common malignant tumors among women worldwide， with an increasing incidence rate year by year， making it a significant public health concern. With the continuous advancement of tumor biology research， N⁶-methyladenosine （m⁶A） modification， as an important form of RNA modification， has attracted growing attention. The m⁶A modification， the most prevalent RNA modification in eukaryotes， occurs in almost all types of RNA and plays a critical role in the occurrence， progression， and metastasis of breast cancer. It influences cell proliferation， apoptosis， and alterations in the tumor microenvironment， though the specific mechanisms underlying these effects require further in-depth investigation. Moreover， the specific patterns of m⁶A modification demonstrate its potential as a novel biomarker for breast cancer， which could provide new directions for early diagnosis and prognosis evaluation.

Key words: Breast neoplasms, Epigenomics, N⁶-methyladenosine

郭俊龙, 邹睿琪, 陈少强, 梁雨欣, 李菁, 雍苏南, 何玉婷, 谢小兵, 李萍. RNA m⁶A修饰在乳腺癌中的研究进展[J]. 国际肿瘤学杂志, 2025, 52(8): 532-537.

Guo Junlong, Zou Ruiqi, Chen Shaoqiang, Liang Yuxin, Li Jing, Yong Sunan, He Yuting, Xie Xiaobing, Li Ping. Research progress of RNA m⁶A modification in breast cancer[J]. Journal of International Oncology, 2025, 52(8): 532-537.

图/表 1

表1

乳腺癌中m6A修饰常见的调节方式及其机制"

项目	m⁶A相关基因	m⁶A修饰类型	靶基因	机制
细胞增殖	METTL3	writer	piRNA-31106	促进MDM2、CDK4和cyclinD1的表达^[24]
			lncRNA WFDC21P	通过WFDC21P/miR-628/SMAD3信号通路进行调节^[25]
			circMETTL3	通过circMETTL3/miR-31-5p/CDK1信号通路进行调节^[26]
			LINC00520	作为miR-577的竞争性内源RNA进行调节^[27]
	METTL3 YTHDF1	writer reader	ADAR1	通过METTL3/ARHGAP5/YTHDF1信号通路进行调节^[28]
	HNRNPC	reader	miR-944	BACH2通过分子海绵作用刺激HNRNPC表达、通过MAPK信号通路促进肿瘤细胞增殖^[29]
细胞侵袭、转移	METTL3	writer	ZNF217	通过miR-135/ZNF217/METTL3/NANOG信号通路抑制乳腺癌上皮间质转化的启动^[30]
			miR-34c-3p	METTL3通过分子海绵作用抑制细胞增殖、侵袭、肿瘤生长和转移^[31]
			KRT7	通过促进KRT7-AS/KRT7 mRNA双链体的形成以及KRT7的翻译以促进乳腺癌的肺转移^[32]
	METTL14	writer	miR‑146a‑5p	促进miR-146a-5p的高表达，促进乳腺癌细胞的迁移和侵袭^[33]
	FTO	eraser	miR-181b-3p	通过FTO/miR-181b-3p/ARL5B信号通路促进乳腺癌细胞的迁移和侵袭^[34]
	YTHDF1	reader	FOXM1	YTHDF1通过识别并结合m⁶A修饰的FOXM1 mRNA，加速FOXM1的翻译过程，促进乳腺癌细胞的转移^[35]
生物代谢	WTAP	writer	ENO1	C5aR1阳性嗜中性粒细胞通过ERK1/2-WTAP依赖性ENO1的m⁶A 修饰诱导乳腺癌糖酵解^[36]
	METTL3 YTHDF2	writer、reader	LATS1	增强LATS1 mRNA表达以促进糖酵解过程^[37]
	YTHDF1	reader	PKM2	肿瘤缺氧诱导HIF1α转录，抑制miR-16-5p表达，促进YTHDF1的表达，进而通过上调PKM2促进糖酵解^[38]
细胞死亡	METTL14	writer	LINC00942	通过LINC00942-METTL14-CXCR4/CYP1B1信号通路抑制乳腺癌细胞凋亡^[39]
			lncRNA UCA1	通过METTL14/miR-375/SOX12信号通路抑制乳腺癌细胞凋亡^[40]
	FTO	eraser	eIF4G1	5'-tRF-GlyGCC直接结合FTO，并增加FTO去甲基化酶的活性，降低eIF4G1甲基化，抑制自噬^[41]
肿瘤微环境	YTHDF1	reader		与MYC信号调控和T细胞分化有关^[42]
肿瘤微环境	IGF2BP1	reader	lncRNA KB-1980E6.3	通过lncRNA KB-1980E6.3/IGF2BP1/c-Myc信号通路促进乳腺癌干细胞在体外和体内缺氧微环境下的自我更新和肿瘤发生^[43]

表1

参考文献 56

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RNA m⁶A修饰在乳腺癌中的研究进展

Research progress of RNA m⁶A modification in breast cancer

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