LncRNA GAS5 modulates the progression of non-small cell lung cancer through repressing miR-221-3p and up-regulating IRF2
| Autor: | Haiyun Zhang, Huan Zhao, Feifan Xu, Haiyan Miao, Juan Ma, Jing Da, Jingjing Ren, Shengyan Qu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Male Pathology medicine.medical_specialty Histology Lung Neoplasms lncRNA GAS5 Adenocarcinoma of Lung Biology NSCLC Pathology and Forensic Medicine 03 medical and health sciences 0302 clinical medicine Western blot Cell Movement Carcinoma Non-Small-Cell Lung medicine RB1-214 Humans Neoplasm Invasiveness Lung cancer Cell Proliferation A549 cell Reporter gene medicine.diagnostic_test Research Cell migration General Medicine IRF2 medicine.disease miR-221-3p respiratory tract diseases Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Cell culture A549 Cells 030220 oncology & carcinogenesis Cancer research Carcinoma Squamous Cell Disease Progression Female RNA Long Noncoding GAS5 Interferon Regulatory Factor-2 Signal Transduction |
| Zdroj: | Diagnostic Pathology Diagnostic Pathology, Vol 16, Iss 1, Pp 1-9 (2021) |
| ISSN: | 1746-1596 |
| Popis: | Background Long non-coding RNA growth arrest specific 5 (GAS5) is a regulator in non-small cell lung cancer (NSCLC) progression. Nonetheless, the mechanism by which GAS5 exerts its biological function in NSCLC cells remains unclear. Methods GAS5, miR-221-3p relative expression levels in NSCLC tissues and cells were examined by qPCR. After gain-of-function and loss-of-function models were established, the viability of H1299 and A549 cells were examined by CCK-8 and EdU assays. Cell migration and invasion were examined by the Transwell experiment. The binding sequence of GAS5 for miR-221-3p was confirmed by the dual-luciferase reporter gene experiment. The regulatory function of GAS5 and miR-221-3p on IRF2 was investigated by Western blot. Results GAS5 expression was down-modulated in NSCLC tissues and cell lines. GAS5 overexpression restrained the proliferation, migration and invasion of NSCLC cells, while miR-221-3p, which was targeted and negatively modulated by GAS5, worked oppositely. Restoration of miR-221-3p markedly reversed the effects of GAS5 on NSCLC cells. Additionally, GAS5 increased IRF2 expression in NSCLC cells by repressing miR-221-3p. Conclusions GAS5 blocks the progression of NSCLC partly via increasing IRF2 expression level via repressing miR-221-3p. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full text from SpringerLink