LncRNA MACC1-AS1 facilitates the cell growth of small cell lung cancer by sequestering miR-579-3p and mediating NOTCH1-pathway

被引:0
|
作者
Hong, Jiang [1 ]
Gu, Rentong [2 ]
Cheng, Wen [1 ]
Lu, Chaojing [1 ]
Wang, Xiaowei [1 ]
机构
[1] Naval Med Univ, Dept Thorac Surg, Changhai Hosp, Shanghai 200433, Peoples R China
[2] Naval Med Univ, Affiliated Hosp 3, Dept Thorac Surg, Shanghai 200438, Peoples R China
关键词
MACC1-AS1; miR-579-3p; NOTCH1; Small cell lung cancer; PROMOTES; PROGRESSION; MICRORNA;
D O I
10.1016/j.ijbiomac.2024.136579
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
As reported, long non-coding RNAs (lncRNAs) have been confirmed to be of great importance in regulating the progression of diseases, especially of cancers. LncRNA MACC1 antisense RNA 1 (MACC1-AS1) has been studied in some cancers, whereas its biological role and underlying mechanism is still unclear in small cell lung cancer (SCLC). In the current research, we found high level of MACC1-AS1 in SCLC cells. Subsequently, it was discovered that MACC1-AS1 knockdown considerably restrained the proliferative and migratory ability of SCLC cells by inducing the apoptosis. Importantly, the knockdown of MACC1-AS1 inhibited protein levels of genes of NOTCH pathway, and NOTCH pathway activator (Jagged1) countervailed the inhibition of MACC1-AS1 depletion on SCLC cell growth. Further, the deficiency of NOTCH1 hampered SCLC cell growth. More importantly, miR-579-3p was identified as a downstream gene of MACC1-AS1 and thereby targeted to NOTCH1. In addition, miR-579-3p repression recovered the suppressive role of MACC1-AS1 knockdown in NOTCH1 expression. Rescue assays indicated that repressed SCLC cell growth caused by MACC1-AS1 knockdown could be reserved by miR579-3p repression or NOTCH1 overexpression. In brief, lncRNA MACC1-AS1 boosted SCLC cell growth via sequestering miR-579-3p and mediating NOTCH1-pathway.
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页数:8
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