文献类型：期刊文献

英文题名：Long non-coding RNA LSAMP-1 is down-regulated in non-small cell lung cancer and predicts a poor prognosis

作者：Gong, Wei[1,2,7,8];Li, Yinyan[2];Xian, Jianfeng[2];Yang, Lei[1,2];Wang, Yuanyuan[2];Zhang, Xin[1];Zhou, Yifeng[3];Wang, Xinhua[4];Qiao, Guibin[5];Chen, Cuiyi[6];Datta, Soham[2];Gao, Xincheng[1,7,8];Lu, Jiachun[1,2];Qiu, Fuman[1,2]

第一作者：Gong, Wei

通信作者：Lu, JC[1];Qiu, FM[1];Lu, JC[2];Qiu, FM[2]

机构：[1]Guangzhou Med Univ, Affiliated Hosp 1, State Key Lab Resp Dis, 151 Yanjiangxi Rd, Guangzhou 510120, Peoples R China;[2]Guangzhou Med Univ, Sch Publ Hlth, Inst Chem Carcinogenesis, Collaborat Innovat Ctr Environm Toxic, Guangzhou 511436, Peoples R China;[3]Soochow Univ, Dept Genet, Med Coll, 1 Shizi Rd, Suzhou 215123, Peoples R China;[4]Gansu Univ Chinese Med, Sch Publ Hlth, 1 Chinese Med Rd, Lanzhou 730101, Gansu, Peoples R China;[5]Guangdong Acad Med, Guangdong Prov Peoples Hosp, Dept Thorac Surg, Guangzhou 510080, Peoples R China;[6]Third Peoples Hosp Dongguan City, Dongguan 523326, Peoples R China;[7]Guangzhou Med Univ, Affiliated Hosp 1, Minimally Invas Surg Ctr, Dept Urol, Guangzhou, Guangdong, Peoples R China;[8]Guangdong Key Lab Urol, Guangzhou, Guangdong, Peoples R China

第一机构：Guangzhou Med Univ, Affiliated Hosp 1, State Key Lab Resp Dis, 151 Yanjiangxi Rd, Guangzhou 510120, Peoples R China

通信机构：[1]corresponding author), Guangzhou Med Univ, Affiliated Hosp 1, State Key Lab Resp Dis, 151 Yanjiangxi Rd, Guangzhou 510120, Peoples R China;[2]corresponding author), Guangzhou Med Univ, Sch Publ Hlth, Inst Chem Carcinogenesis, Collaborat Innovat Ctr Environm Toxic, Guangzhou 511436, Peoples R China.

年份：2022

卷号：22

期号：1

外文期刊名：CANCER CELL INTERNATIONAL

收录：;Scopus(收录号：2-s2.0-85129666666);WOS:【SCI-EXPANDED(收录号:WOS:000791777400004)】；

基金：This study was supported by the National Natural Science Foundation of China 82173609, 81872694, 81673267 (J. Lu), 81872127, 81602289 (F. Qiu), 81273149, 81402753, 81672303 (L. Yang), the National Key R&D Projects (2016YFC0903700), Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program 2017BT01S155(J. Lu), Guangdong High School Young Innovative Talents Project (2015KQNCX136), Guangzhou Science Research Program General Project (201707010123, 201804020023), Guangzhou Municipal Scientific Research Project (1201630073) and Guangzhou Science and Technology Program Pearl River Nova projects Grant 201710010049 (L. Yang). Guangdong education bureau Characteristic innovation project Grants 2015KTSCX116 (L.Yang) and Guangdong Provincial Major Projects Grants 2014KZDXM046, Yangcheng Scholar Grants 1201541589 (J. Lu) and Young and middle-aged scientific research backbone training project of Shenzhen People's Hospital (SYJCYJ202107).

语种：英文

外文关键词：Lnc-LSAMP-1; LSAMP gene; Non-small cell lung cancer (NSCLC); Biomarker; Prognosis; Chemosensitivity

摘要：Background Long noncoding RNAs (lncRNAs) are emerging as master regulators for gene expression and thus play a vital role in human tumorigenesis and progression. But the involvement of novel lncRNAs in non-small cell lung cancer (NSCLC) remains largely unelucidated. Methods A total of 170 NSCLC and their adjacent non-tumor tissues were enrolled to detect the expression of Lnc-LSAMP-1 by RT-qPCR. The effects of Lnc-LSAMP-1 on cell proliferation, migration, invasion and drug-sensitivity were determined by in vitro and in vivo experiments. The proteins that interact with Lnc-LSAMP-1were confirmed by RNA pull-down assay. RNA-sequencing were used to identify the potential targets of Lnc-LSAMP-1 in NSCLC. Results We found that Lnc-LSAMP-1 was significantly down-regulated in 170 cases of NSCLC tissues when compared to their adjacent non-cancerous tissues. Loss expression of Lnc-LSAMP-1 was notably correlated with unfavorable prognosis of NSCLC patients. The ectopic expression of Lnc-LSAMP-1 drastically inhibited lung cancer cell proliferation, viability, invasion and migration ability, arrested cell cycle and facilitated apoptosis. Chemotherapy sensitization experiments showed that over-expressed Lnc-LSAMP-1 enhanced the inhibition of cell proliferation induced by TKI. Mechanistically, Lnc-LSAMP-1-LSAMP formed a complex which could protect the degradation of LSAMP gene, and thus exerted crucial roles in NSCLC progression and TKI targeted treatment. Conclusions Consequently, our findings highlight the function and prognostic value of Lnc-LSAMP-1 in NSCLC and provide potential novel therapeutic targets and prognostic biomarkers for patients with NSCLC.