Comprehensive landscape of epigenetic-dysregulated lncRNAs reveals a profound role of enhancers in carcinogenesis in BC subtypes

癌变 表观遗传学 生物 后生 增强子 癌症研究 计算生物学 转录因子 DNA甲基化 基因 遗传学 癌症 基因表达
作者
Hongying Zhao,Xiaoqin Liu,Lei Yu,Shihua Lin,Caiyu Zhang,Haotian Xu,Zhijun Leng,Waidong Huang,Junjie Lei,Tengyue Li,Jing Li,Fan Yang,Li Wang
出处
期刊:Molecular therapy. Nucleic acids [Elsevier]
卷期号:23: 667-681 被引量:56
标识
DOI:10.1016/j.omtn.2020.12.024
摘要

Aberrant expression of long non-coding RNAs (lncRNA) is associated with altered DNA methylation and histone modifications during carcinogenesis. However, identifying epigenetically dysregulated lncRNAs and characterizing their functional mechanisms in different cancer subtypes are still major challenges for cancer studies. In this study, we systematically analyzed the epigenetic alterations of lncRNAs at important regulatory elements in three breast cancer subtypes. We identified 87, 691, and 1,197 epigenetically dysregulated lncRNAs in luminal, basal, and claudin-low subtypes of breast cancer, respectively. The landscape of epigenetically dysregulated lncRNAs at enhancer elements revealed that epigenetic changes of the majority of lncRNAs occurred in a subtype-specific manner and contributed to subtype-specific biological functions. We identified six acetylation of lysine 27 on histone H3 (H3K27ac)-dysregulated lncRNAs and three DNA methylation-dysregulated lncRNAs (CTC-303L1.2, RP11-738B7.1, and SLC26A4-AS1) as prognostic biomarkers of basal subtype. These lncRNAs were involved in immune response-related biological functions. Treatment of the basal breast cancer cell line MDA-MB-468 with CREBBP/EP300 bromodomain inhibitors downregulated H3K27 acetylation levels and caused a decrease in the expression of five H3K27ac-dysregulated lncRNAs (LINC00393, KB-1836B5.1, RP1-140K8.5, AC005162.1, and AC020916.2) and inhibition of the growth of breast cancer cells. One epigenetically dysregulated lncRNA (LINC01983) and four lncRNA regulators (UCA1, RP11-221J22.2, RP11-221J22.1, and RP1-212P9.3) were identified as prognostic biomarkers of the luminal molecular subtype of breast cancer by controlling the tumor necrosis factor (TNF) signaling pathway, T helper (Th)17 cell differentiation, and T cell migration. Finally, our results highlighted a profound role of enhancer-related H3K27ac-dysregulated lncRNAs, DNA methylation-dysregulated lncRNAs, and lncRNA regulators in breast cancer subtype carcinogenesis and their potential prognostic value. Aberrant expression of long non-coding RNAs (lncRNA) is associated with altered DNA methylation and histone modifications during carcinogenesis. However, identifying epigenetically dysregulated lncRNAs and characterizing their functional mechanisms in different cancer subtypes are still major challenges for cancer studies. In this study, we systematically analyzed the epigenetic alterations of lncRNAs at important regulatory elements in three breast cancer subtypes. We identified 87, 691, and 1,197 epigenetically dysregulated lncRNAs in luminal, basal, and claudin-low subtypes of breast cancer, respectively. The landscape of epigenetically dysregulated lncRNAs at enhancer elements revealed that epigenetic changes of the majority of lncRNAs occurred in a subtype-specific manner and contributed to subtype-specific biological functions. We identified six acetylation of lysine 27 on histone H3 (H3K27ac)-dysregulated lncRNAs and three DNA methylation-dysregulated lncRNAs (CTC-303L1.2, RP11-738B7.1, and SLC26A4-AS1) as prognostic biomarkers of basal subtype. These lncRNAs were involved in immune response-related biological functions. Treatment of the basal breast cancer cell line MDA-MB-468 with CREBBP/EP300 bromodomain inhibitors downregulated H3K27 acetylation levels and caused a decrease in the expression of five H3K27ac-dysregulated lncRNAs (LINC00393, KB-1836B5.1, RP1-140K8.5, AC005162.1, and AC020916.2) and inhibition of the growth of breast cancer cells. One epigenetically dysregulated lncRNA (LINC01983) and four lncRNA regulators (UCA1, RP11-221J22.2, RP11-221J22.1, and RP1-212P9.3) were identified as prognostic biomarkers of the luminal molecular subtype of breast cancer by controlling the tumor necrosis factor (TNF) signaling pathway, T helper (Th)17 cell differentiation, and T cell migration. Finally, our results highlighted a profound role of enhancer-related H3K27ac-dysregulated lncRNAs, DNA methylation-dysregulated lncRNAs, and lncRNA regulators in breast cancer subtype carcinogenesis and their potential prognostic value.

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
1秒前
崔鹤然完成签到,获得积分10
1秒前
欢喜小蚂蚁完成签到 ,获得积分10
2秒前
2秒前
风的味道完成签到,获得积分10
2秒前
bkagyin应助我寄人间雪满头采纳,获得10
2秒前
郭浩峰完成签到,获得积分10
2秒前
茄子完成签到,获得积分10
3秒前
空城完成签到,获得积分10
3秒前
grs完成签到,获得积分10
3秒前
125完成签到,获得积分10
4秒前
1234完成签到 ,获得积分10
4秒前
堂yt发布了新的文献求助10
4秒前
Richard完成签到 ,获得积分10
4秒前
真实的新瑶完成签到,获得积分10
5秒前
不安的傲白完成签到,获得积分10
5秒前
在水一方应助房天川采纳,获得10
5秒前
6秒前
天想月完成签到,获得积分10
6秒前
grs发布了新的文献求助10
7秒前
苍耳君完成签到,获得积分10
7秒前
kol完成签到,获得积分10
7秒前
Doris完成签到,获得积分10
7秒前
賢様666完成签到,获得积分10
8秒前
老迟到的友菱完成签到,获得积分10
8秒前
czzlancer完成签到,获得积分10
8秒前
恸0325完成签到,获得积分10
8秒前
岁岁平安完成签到,获得积分10
9秒前
2052669099应助香蕉君采纳,获得10
9秒前
spz150完成签到,获得积分10
9秒前
初学者完成签到,获得积分10
9秒前
李周发布了新的文献求助10
9秒前
苗条馒头完成签到,获得积分10
9秒前
852应助柠静樨采纳,获得30
9秒前
Tiffy完成签到,获得积分10
9秒前
Ps完成签到 ,获得积分10
10秒前
香菜大姐完成签到,获得积分10
10秒前
10秒前
酆百川完成签到,获得积分10
10秒前
cxl完成签到,获得积分10
11秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Handbook of pharmaceutical excipients, Ninth edition 5000
Aerospace Standards Index - 2026 ASIN2026 3000
Polymorphism and polytypism in crystals 1000
Signals, Systems, and Signal Processing 610
Discrete-Time Signals and Systems 610
T/SNFSOC 0002—2025 独居石精矿碱法冶炼工艺技术标准 600
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 纳米技术 有机化学 物理 生物化学 化学工程 计算机科学 复合材料 内科学 催化作用 光电子学 物理化学 电极 冶金 遗传学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 6043296
求助须知:如何正确求助?哪些是违规求助? 7804737
关于积分的说明 16238788
捐赠科研通 5188809
什么是DOI,文献DOI怎么找? 2776749
邀请新用户注册赠送积分活动 1759786
关于科研通互助平台的介绍 1643319