Long non-coding RNA HAGLROS facilitates the malignant phenotypes of NSCLC cells via repressing miR-100 and up-regulating SMARCA5
| Autor: | Yaoqi Ke, Shuai Yang, Qingping Cheng, Hongyan Zhu, Li Li, Xiangyang Li |
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| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Lung Neoplasms Chromosomal Proteins Non-Histone Biology law.invention 03 medical and health sciences 0302 clinical medicine Western blot Cell Movement law Carcinoma Non-Small-Cell Lung medicine Humans Polymerase chain reaction Cell Proliferation Adenosine Triphosphatases Gene knockdown Reporter gene medicine.diagnostic_test RNA General Medicine Phenotype Long non-coding RNA respiratory tract diseases Gene Expression Regulation Neoplastic MicroRNAs 030104 developmental biology Cell culture 030220 oncology & carcinogenesis Cancer research RNA Long Noncoding |
| Zdroj: | Biomedical Journal. 44:S305-S315 |
| ISSN: | 2319-4170 |
| Popis: | Background Long non-coding RNA (lncRNA) is implicated in the progression of multiple cancers. This study aimed to explore the expression characteristics, biological function and molecular mechanism of lncRNA HAGLROS expression in NSCLC. Methods Quantitative real-time polymerase chain reaction (RT-PCR) was adopted to detect HAGLROS expression in NSCLC tissues and normal lung tissues. Survival curve was plotted by Kaplan–Meier method. Gain-of-function and loss-of-function models were respectively established to investigate the biological functions of HAGLROS, miR-100 and SMARCA5. MTT and Transwell assays were carried out to monitor the changes in proliferation, migration and invasion of NSCLC cells. Bioinformatics analysis and dual-luciferase reporter assay were used to verify the binding sites between HAGLROS and miR-100. Western blot was performed to determine the regulatory effects of HAGLROS and miR-100 on SMARCA5 protein expression. Results Up-regulated HAGLROS expression was observed in NSCLC tissues and cell lines. Over-expressed HAGLROS promoted the malignant phenotypes of NSCLC cells; conversely, HAGLROS knockdown repressed the malignant phenotypes of NSCLC cells. HAGLROS repressed miR-100 expression to promote SMARCA5 expression in NSCLC cells, and miR-100 overexpression or SMARCA5 knockdown counteracted the oncogenic functions of HAGLROS. Conclusions These results conclude that HAGLROS is a tumor promoter in NSCLC, and it regulates the malignant phenotypes of NSCLC cells via miR-100/SMARCA5 axis. |
| Databáze: | OpenAIRE |
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