Functions of long non-coding RNA LNC11649 in non-small cell lung cancer cells as a reprocessed form of MALAT1

作者全名："Qi, Jun-Zhe; Zhao, Ting -Ting; Qi, Shu-Shan"

作者地址："[Qi, Jun-Zhe] Chongqing Med Univ, Dept Clin Med, Chongqing, Peoples R China; [Zhao, Ting -Ting; Qi, Shu-Shan] Liangxiang Hosp Beijing Fangshan Dist, Dept Thorac Surg, Beijing, Peoples R China"

通信作者："Qi, SS (通讯作者)，Liangxiang Hosp Beijing Fangshan Dist, Dept Thorac Surg, Beijing, Peoples R China."

来源：NEOPLASMA

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000950382400007

JCR分区：Q3

影响因子：3

年份：2022

卷号：69

期号：6

开始页：1322

结束页：+

文献类型：Article

关键词：Key words; lncRNA; non -small cell lung cancer; MALAT1; LNC11649; MSI1

摘要："Long non-coding RNAs (lncRNAs) have received much attention concerning their expression mechanisms in tumor formation. It is known that lncRNAs are involved in the occurrence, development, and prognosis of various tumors, including lung cancer. In our study, one non-coding RNA, LNC11649 (649 nt in length), was identified in non-small cell lung cancer (NSCLC) by PacBio third-generation sequencing technology. Both northern blot and quantitative PCR analyses confirmed the presence of LNC11649 in NSCLC tissues and cells with high expression. Its sequence was found to be highly homologous to lncRNA MALAT1. Knocking down MALAT1 could lead to a significant downregulation of LNC11649 content, revealing the possibility that LNC11649 could originate from MALAT1 reprocessing. RNA immunoprecipitation and electrophoretic mobility shift assays confirmed an interaction between LNC11649 and the MSI1 protein. Further experiments revealed that LNC11649 promoted the cytoplasmic distribution of MSI1 through its interaction with MSI1 and then activated the Akt signaling pathway to regulate the proliferation and migration of NSCLC cells. Our study reveals the possibility that LNC11649 plays a cancer-promoting role as a reprocessed form of MALAT1 in NSCLC cells and suggests that the MALAT1/LNC11649/MSI1/Akt regulatory axis becomes a potential therapeutic target for lung cancer."

基金机构：Scientific Research Subject of Liangxiang Hospital [2017-02]

基金资助正文：This work is supported by the Scientific Research Subject of Liangxiang Hospital (Grant no. 2017-02).