hsa_circ_0062389 promotes the progression of non-small cell lung cancer by sponging miR-103a-3p to mediate CCNE1 expression
| Autor: | Guangting Zhou, Yahui She, Tan Yang, Zuojun Shen, Fangyan Jia, Yuanyuan Han |
|---|---|
| Rok vydání: | 2020 |
| Předmět: |
Cancer Research
Lung Neoplasms Carcinogenesis Biology medicine.disease_cause Metastasis 03 medical and health sciences 0302 clinical medicine Cell Movement Carcinoma Non-Small-Cell Lung Cell Line Tumor Cyclin E Genetics medicine Humans RNA Small Interfering Pneumonectomy Lung cancer Lung Molecular Biology Cell Proliferation Oncogene Proteins RNA Circular Cell cycle medicine.disease G1 Phase Cell Cycle Checkpoints Up-Regulation respiratory tract diseases Cancer treatment Gene Expression Regulation Neoplastic MicroRNAs Cell culture Tumor progression 030220 oncology & carcinogenesis Disease Progression Cancer research Non small cell |
| Zdroj: | Cancer Genetics. 241:12-19 |
| ISSN: | 2210-7762 |
| DOI: | 10.1016/j.cancergen.2019.12.004 |
| Popis: | Recently, increasing evidence showed that circular RNAs (circRNAs) play critical roles in tumor progression. However, the roles of hsa_circ_0062389 in non-small cell lung cancer (NSCLC) development remain unclear. In the present study, hsa_circ_0062389 expression was significantly increased in NSCLC tissues and cell lines. High hsa_circ_0062389 expression was associated with advanced TNM stage and lymph-node metastasis. Function assays showed that hsa_circ_0062389 suppression reduced NSCLC cells proliferation and arrested cell cycle in G0/G1 phase. In mechanism, hsa_circ_0062389 directly interacted with miR-103a-3p in NSCLC, and CCNE1 acted as a target of miR-103a-3p. Furthermore, rescue assays showed that miR-103a-3p suppression or CCNE1 overexpression abolished the effects of hsa_circ_0062389 suppression on lung cancer cells progression. Therefore, our results showed that the hsa_circ_0062389/miR-103a-3p/CCNE1 axis might contribute to the tumorigenesis of NSCLC, which provided a new strategy for cancer treatment. |
| Databáze: | OpenAIRE |
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