Exploring the Role of Circular RNA (Circ_0001806) in Non-Small Cell Lung Cancer Progression and Immune Evasion through miRNA Regulation

Author:

Guo Yuhong1,Meng Lingchen2,Liang Xiao3,Hou Zhaohui4,Leng Wenping5,Sun Yue6,Yang Yuanshuo6,Hou Zhenbo7,Zhang Peng2

Affiliation:

1. Department of Pathology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Centre for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin, Tianjin’s Clinical Research Centre for Cancer, Tianjin 300060, China

2. Department of Cardiothoracic Surgery, Tianjin Medical University General Hospital, Tianjin 300052, China

3. Department of Thoracic Surgery, Zibo Central Hospital, Zibo, Shandong, 255000, China

4. Department of Colorectal Surgery, Chifeng Baoshan Hospital, Chifeng, Inner Mongolia, 024000, China

5. Department of Neurology, Zibo Maternal and Child Health Hospital (Zibo Third People’s Hospital/Zibo Women and Children’s Hospital), Zibo, Shandong, 255000, China

6. Department of Pathology, Zibo Central Hospital, Zibo, Shandong, 255000, China

7. Department of Pathology, Zibo Maternal and Child Health Hospital (Zibo Third People’s Hospital/Zibo Women and Children’s Hospital), Zibo, Shandong, 255000, China

Abstract

CircRNAs are a class of endogenous non-coding RNAs. Therefore, circRNA has the potential to be used as a molecular marker in tumor therapy. The aim of this study is to detect the important functions of circ_0001806 on the progress and immune escape NSCLC. RT-QPCR was used to calculate the levels of circRNA and miRNA. Immunoblotting was employed to measure the protein level of PDL1. MTT and transwell assays were applied to detect the cell proliferation, migration and invasion. We found that knockdown circ_0001806 inhibited cell proliferation, migration, invasion and suppressed PDL1 expression of NSCLC. Circ_0001806 directly binding to miR-1236, and miR-1236 could partially reversed the functions of silencing circ_0001806. Circ_0001806 regulated cell proliferation, migration, invasion, and tumor immune escape by sponging miR-1236, providing a new perspective for exploring targeted therapies for NSCLC.

Publisher

American Scientific Publishers

Subject

General Materials Science

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