Long noncoding RNA CERS6-AS1 functions as a malignancy promoter in breast cancer by binding to IGF2BP3 to enhance the stability of CERS6 mRNA

被引:61
作者
Bao, Gang [1 ]
Huang, Jianjun [1 ]
Pan, Wei [2 ]
Li, Xing [2 ]
Zhou, Tian [1 ]
机构
[1] Guizhou Med Univ, Breast Surg, Affiliated Hosp, 28 Guiyi St, Guiyang 550004, Guizhou, Peoples R China
[2] Guizhou Med Univ, Inspect Inst, Guiyang, Guizhou, Peoples R China
来源
CANCER MEDICINE | 2020年 / 9卷 / 01期
关键词
breast cancer; CERS6; CERS6-AS1; IGF2BP3; CELL-GROWTH; PROTEIN; SPHINGOLIPIDS; PATHOGENESIS;
D O I
10.1002/cam4.2675
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Breast cancer (BC) leads to the highest mortality in women worldwide, characterized by inevitable proliferation and metastasis of BC cells. Mounting evidence confirm that lncRNAs play a significant role in the tumorigenesis and development of BC. lncRNA CERS6-AS1 is a novel discovery, and its role and molecular mechanism in BC has not been studied. In this study, it was discovered that CERS6-AS1 was overexpressed in BC tissues and cells. CERS6-AS1 accelerated cell proliferation and suppressed cell apoptosis in BC. Moreover, molecular mechanism exploration uncovered that there was a positive association between CERS6 and CERS6-AS1 (or IGF2BP3) expression in BC. Furthermore, IGF2BP3 serves as a RNA-binding protein for CERS6-AS1 and CERS6-AS1 promoted CERS6 mRNA stability by binding to IGF2BP3. In the end, rescue experiments verified that overexpression of CERS6 rescues the inhibition of CERS6-AS1 deficiency on BC progression in vitro and vivo. Taken together, these evidences suggested that CERS6-AS1 promoted the progression of BC by binding to IGF2BP3 and thus enhancing the stability of CERS6 mRNA, providing a new underlying therapeutic target for BC to improve prognosis.
引用
收藏
页码:278 / 289
页数:12
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