Dataset Information

Novel long non-coding RNA LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma.

ABSTRACT: BACKGROUND:We have previously developed a unique metastasis-associated signature consisting of six long non-coding RNAs (lncRNAs), including a novel lncRNA, namely LINC02323. In the present study, we aimed to investigate the underlying roles of LINC02323 in the migration, invasion and TGF-?-induced epithelial-mesenchymal transition (EMT) of lung adenocarcinoma (LUAD) cells. METHODS:The distribution of LINC02323 was detected by the nuclear-plasma separation experiment. Cell proliferation was assessd by MTT assay, and cell migration and invation were detected by transwell assays. EMT was detected by RT-qPCR and western blotting. Interaction between miRNA and LINC02323 was predicted by starBase v2.0 and confirmed by the double luciferase reporting system. RESULTS:LINC02323 was distributed in the cytoplasm and nucleus. The overexpression or deletion of LINC02323 did not affect the proliferation of LUAD cells, while significantly affected the migration and invasion of LUAD cells. TGF-?-induced EMT process was significantly affected by both RNA interference (RNAi) and overexpression of LINC02323. The predicted results showed that there were binding sites between LINC02323 and miR-1343-3p. The expression of LINC02323 was found to be negatively correlated with miR-1343-3p in LUAD by analyzing The Cancer Genome Atlas (TCGA) database. The double luciferase reporting system, RT-qPCR and western blotting experiments confirmed that LINC02323 could bind to miR-1343-3p, which bound to TGF-? receptor 1 (TGFBR1). Inhibition of miR-1343-3p reversed LINC02323 silencing-mediated suppression of migration, invasion and EMT. CONCLUSIONS:LINC02323 acts as a competing endogenous RNA (ceRNA), which sponged miR-1343-3p to upregulate the TGFBR1 expression and promote the EMT and metastasis in LUAD. KEY POINTS:SIGNIFICANT FINDINGS OF THE STUDY: LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma. WHAT THIS STUDY ADDS:LINC02323 is a key molecule in the process of invasion and metastasis of LUAD and might be used as a potential target in metastatic cancer.

SUBMITTER: Zhang X

PROVIDER: S-EPMC7471025 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Novel long non-coding RNA LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma.

Zhang Xiaoshi X Du Lutao L Han Jingyi J Li Xiaoli X Wang Hongchun H Zheng Guixi G Wang Yunshan Y Yang Yongmei Y Hu Ying Y Wang Chuanxin C

Thoracic cancer 20200709 9

<h4>Background</h4>We have previously developed a unique metastasis-associated signature consisting of six long non-coding RNAs (lncRNAs), including a novel lncRNA, namely LINC02323. In the present study, we aimed to investigate the underlying roles of LINC02323 in the migration, invasion and TGF-β-induced epithelial-mesenchymal transition (EMT) of lung adenocarcinoma (LUAD) cells.<h4>Methods</h4>The distribution of LINC02323 was detected by the nuclear-plasma separation experiment. Cell prolife ...[more]

PMID: 32643848

Similar Datasets

Project description:Epithelial ovarian cancer (EOC) is one of the most frequent and fatal gynecologic malignant tumors resulting in an unsatisfying prognosis. Long non-coding RNAs (lncRNAs) play pivotal roles in the tumorigenesis and progression of EOC. However, the profile of lncRNAs involved in EOC remains to be expanded to further improve clinical treatment strategy. In present study, we identified a novel tumor-suppressive lncRNA small nucleolar RNA host gene 10 (SNHG10) in EOC. Kaplan-Meier analysis and COX proportional hazard progression model showed that low expression of SNHG10 was correlated with a poor prognosis of EOC patients. Overexpressing SNHG10 suppressed the proliferation, colony formation, migration, and invasion of EOC cells. Furthermore, SNHG10 was predicted to sponge miR-200a-3p in EOC cells according to the LncBase v.2 experimental module. Then, the binding of SNHG10 and miR-200a-3p was confirmed by performing quantitative real-time PCR (qRT-PCR) and luciferase reporter assays. RNA immunoprecipitation (RIP) showed that SNHG10 and miR-200a-3p occupied the same Ago2 protein to form an RNA-induced silencing complex (RISC). By overlapping the results from the bioinformatics algorithms, tumor-suppressor bridging integrator-1 (BIN1) was found to be a main downstream target of the SNHG10/miR-200a-3p axis. Low expression of BIN1 in EOC tissues was detected by using immunohistochemistry (IHC). Besides, BIN1 and SNHG10 expression was positively correlated in EOC tissues. By performing miRNA rescue experiments, a SNHG10/miR-200a-3p/BIN1 axis and its promoting effects on malignant behaviors and epithelial-mesenchymal transition (EMT) process were verified in EOC cells. Moreover, SNHG10 overexpression significantly suppressed the tumorigenesis and EMT of EOC cells in vivo. Altogether, SNHG10 sponges miR-200a-3p to upregulate BIN1 and thereby exerting its tumor-suppressive effects in EOC. Therefore, the SNHG10/miR-200a-3p/BIN1 axis may act as a potential predictive biomarker and therapeutic target for treating EOC.

Dataset Information

Novel long non-coding RNA LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma.

Publications

Novel long non-coding RNA LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets