基因沉默
细胞生长
癌症研究
转染
基因敲除
竞争性内源性RNA
生物
肺癌
小RNA
细胞
GRB2型
下调和上调
细胞培养
信号转导
医学
肿瘤科
细胞生物学
长非编码RNA
原癌基因酪氨酸蛋白激酶Src
基因
遗传学
作者
Wei Wei,Changyong Wang,Jianfeng Zhang,Xun Hu,Lei Wei,Hairong Huang
出处
期刊:Combinatorial Chemistry & High Throughput Screening
[Bentham Science]
日期:2023-08-01
卷期号:26 (10): 1836-1847
被引量:1
标识
DOI:10.2174/1386207325666220624093957
摘要
Background: Non-small cell lung cancer (NSCLC) is associated with high morbidity and mortality. Dysregulation of lncRNAs leads to NSCLC progression. Objective: This study aims to explore the regulatory mechanism of lncRNA LINC01234 in NSCLC. Materials and Methods: LINC01234 expression in NSCLC cells was determined. Cell proliferation was detected using CCK-8, colony formation, and EDU assays after transfection of siRNA LINC01234 into H1299 cells and transfection of pcDNA3.1-LINC01234 into H1975 cells. Subcellular localization of LINC01234 was predicted and the binding relations between LINC01234 and miR-433-3p as well as miR-433-3p and GRB2 were verified. The expression levels of miR-433-3p and GRB2 in NSCLC cells were determined. Joint experiments of miR-433-3p inhibitor + si- LINC01234-1 or oe-GRB2 + si-LINC01234-1 were conducted to verify the role of miR-433-3p and GRB2 in NSCLC cell malignant proliferation. Results: LINC01234 was abundantly expressed in NSCLC cells. LINC01234 silencing reduced NSCLC cell proliferation while LINC01234 overexpression enhanced cell proliferation. LINC01234 competitively bound to miR-433-3p and miR-433-3p directly targeted GRB2. miR- 433-3p knockdown or GRB2 overexpression counteracted the repressive effect of LINC01234 silencing on NSCLC cell malignant proliferation. Conclusion: LINC01234 competitively bound to miR-433-3p and promoted GRB2 transcription to augment NSCLC cell malignant proliferation.
科研通智能强力驱动
Strongly Powered by AbleSci AI