Hsa_circ_0092856 Promoted the Proliferation, Migration, and Invasion of NSCLC Cells by Up-Regulating the Expression of eIF3a

Author:

Yuan Fuqiang12,Huang Masha123,Huang Hanxue12,Mao Xiaoyuan12ORCID,Xie Pan12,Li Xi12,Gao Yang4ORCID,Zeng Feiyue5,Liu Zhaoqian12

Affiliation:

1. Hunan Key Laboratory of Pharmacogenetics, Department of Clinical Pharmacology, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Changsha 410008, China

2. Institute of Clinical Pharmacology, Engineering Research Center for Applied Technology of Pharmacogenomics of Ministry of Education, Central South University, Changsha 410078, China

3. Department of Biochemistry and Molecular Cell Biology, College of Basic Medical Sciences, School of Medicine, Shanghai Jiao Tong University, Shanghai 200025, China

4. Department of Thoracic Surgery, Xiangya Hospital, Central South University, Changsha 410008, China

5. Department of Radiology, Xiangya Hospital, Central South University, Changsha 410008, China

Abstract

Circular RNA (circRNA) plays a very important regulatory role in a variety of human malignancies such as non-small-cell lung cancer (NSCLC). In the current study, we explored the role of hsa_circ_0092856 in the progression of NSCLC. We screened CircRNA from the eIF3a gene in the Circbase database. The biological functions of hsa_circ_0092856 in NSCLC were analyzed via qRT-PCR, a CCK-8 assay, a plate cloning experiment, scratch testing, a transwell chamber experiment, an RNA nuclear mass separation experiment, an RIP experiment, and a Western blot test. The results showed that hsa_circ_0092856 was highly expressed in NSCLC cells, and the knockdown of hsa_circ_0092856 could inhibit the proliferation, migration, and invasion of NSCLC cells. The overexpression of hsa_circ_0092856 has the opposite effect. The expression of eIF3a also changed with the change in hsa_circ_0092856. These results suggest that hsa_circ_0092856 may play a key role in the progression of NSCLC by regulating the expression of eIF3a.

Funder

National Natural Science Foundation of China

Publisher

MDPI AG

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