Novel long non-coding RNA LINC02323 promotes epithelial-mesenchymal transition and metastasis via sponging miR-1343-3p in lung adenocarcinoma
Autor: | Xiaoli Li, Xiaoshi Zhang, Yunshan Wang, Guixi Zheng, Ying Hu, Yongmei Yang, Lutao Du, Hongchun Wang, Jingyi Han, Chuanxin Wang |
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Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Pulmonary and Respiratory Medicine Epithelial-Mesenchymal Transition Lung Neoplasms Adenocarcinoma of Lung Transfection lcsh:RC254-282 Metastasis 03 medical and health sciences 0302 clinical medicine TGF‐β receptor 1 RNA interference microRNA medicine Humans Epithelial–mesenchymal transition Neoplasm Metastasis business.industry Competing endogenous RNA LINC02323 Cell migration General Medicine Original Articles lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens medicine.disease lung adenocarcinoma Long non-coding RNA MicroRNAs 030104 developmental biology Oncology 030220 oncology & carcinogenesis Cancer research Adenocarcinoma RNA Long Noncoding Original Article Epithelial‐mesenchymal transition business miR‐1343‐3p |
Zdroj: | Thoracic Cancer Thoracic Cancer, Vol 11, Iss 9, Pp 2506-2516 (2020) |
ISSN: | 1759-7714 |
Popis: | 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‐β‐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‐β‐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‐β 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. 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. |
Databáze: | OpenAIRE |
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