基因敲除
癌症研究
细胞生长
转移
生物
长非编码RNA
肺癌
小RNA
低密度脂蛋白受体
分子生物学
核糖核酸
癌症
细胞培养
医学
基因
肿瘤科
遗传学
脂蛋白
内分泌学
胆固醇
作者
Lijun Wang,Cunzhi Lin,Nina Sun,Qiang Wang,Xiaoqian Ding,Yong Sun
摘要
Abstract Background Non‐small cell lung cancer (NSCLC) is a lethal tumor resulting in a large number of cancer‐related deaths globally. Long noncoding RNAs (lncRNAs) may modulate tumor initiation and metastasis. Although dysregulation of lncRNA cancer susceptibility 19 (CASC19) is validated in NSCLC, further exploration of the CASC19‐regulated mechanism in NSCLC is still needed. Methods CASC19 expression was examined in NSCLC cells by a quantitative reverse transcriptase‐polymerase chain reaction. The specific role of CASC19 in NSCLC was analyzed by cell counting kit‐8, EdU, Transwell and western blot assays. The interaction between miR‐301b‐3p and CASC19 or low‐density lipoprotein receptor (LDLR) was confirmed by luciferase reporter and RNA immunoprecipitation assays. Results CASC19 is markedly overexpressed in NSCLC. Its deficiency impairs cell proliferation, as well as metastasis in NSCLC. Molecular mechanism experiments indicated that CASC19 negatively modulates the expression of miR‐301b‐3p and miR‐301b‐3p can bind with CASC19 in NSCLC. In addition, miR‐301b‐3p binds to LDLR to impair its expression in NSCLC. Finally, rescue experiments showed that miR‐301b‐3p inhibition or LDLR overexpression counteracted the CASC19 knockdown‐mediated function on cell proliferation and metastasis in NSCLC. Conclusions CASC19 facilitates NSCLC cell proliferation and metastasis by targeting the miR‐301b‐3p/LDLR axis, offering a possible strategy for lncRNA‐targeted treatment in NSCLC.
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