circFOXM1 promotes proliferation of non-small cell lung carcinoma cells by acting as a ceRNA to upregulate FAM83D
| Autor: | Haojie Jin, Zhuoan Cheng, Qing Ye, Wenxin Qin, Shaohua Cui, Hui Wang, Xiaowei Mao, Chengtao Yu, Yujie Fu, Xiaojing Zhao, Botai Li, Liyan Jiang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Cancer Research Lung Neoplasms FAM83D Cell miR-614 Cell Cycle Proteins Biology lcsh:RC254-282 03 medical and health sciences 0302 clinical medicine Downregulation and upregulation Non-small cell lung cancer Circular RNA Carcinoma Non-Small-Cell Lung Cell Line Tumor medicine Humans Gene silencing Cell Proliferation Reporter gene Cell growth Competing endogenous RNA Research Forkhead Box Protein M1 RNA circFOXM1 RNA Circular Middle Aged lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens Up-Regulation 030104 developmental biology medicine.anatomical_structure Oncology 030220 oncology & carcinogenesis Cancer research Female Microtubule-Associated Proteins |
| Zdroj: | Journal of Experimental & Clinical Cancer Research, Vol 39, Iss 1, Pp 1-16 (2020) Journal of Experimental & Clinical Cancer Research : CR |
| ISSN: | 1756-9966 |
| Popis: | Background Biological role and clinical significance of circular RNAs (circRNAs) remain largely unknown. Herein, we aimed to investigate biological function, molecular mechanism, and clinical significance of a circular RNA FOXM1 (circFOXM1) in non-small cell lung cancer (NSCLC). Methods Expression of circFOXM1 was measured in 48 paired samples of NSCLC by qRT-PCR. Functional roles of circFOXM1 on tumor cells were explored by in vitro and in vivo assays. Transcriptome sequencing was employed to screen the molecules involved in circFOXM1 regulatory network. RNA immunoprecipitation, luciferase analysis, RNA pull-down, and rescue assay were used to investigate potential mechanisms of circFOXM1. Results We found that circFOXM1 was significantly upregulated in NSCLC tissues, and its upregulation was positively correlated with advanced clinical stage and poor prognosis of NSCLC patients. Gain or loss-of-function assay showed that circFOXM1 promoted cell proliferation and cell cycle progression. In vivo assays showed that silencing circFOXM1 inhibited xenograft tumor growth. Mechanically, transcriptome sequencing data indicated that silencing circFOXM1 led to the downregulation of cell cycle-related mRNAs. RNA pull-down and dual-luciferase reporter assay suggested that circFOXM1 could bind to miR-614, and FAM83D was an essential gene involved in the circFOXM1/miR-614 regulatory network. Conclusions circFOXM1promotes NSCLC progression by interacting with miR-614 and thus inactivating the function of miR-614, which will further release the suppression of FAM83D. circFOXM1/miR-614/FAM83D regulatory network may serve as a potential therapeutic target for NSCLC patients. |
| Databáze: | OpenAIRE |
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