Summary: | Qian Chen,1,2,* Hongyu Zhang,3,4,* Jianyin Zhang,1,2 Le Shen,1,2 Jing Yang,1,2 Yan Wang,1,2 JinXiu Ma,1,2 Bing Zhuan1,2 1Department of Respiratory Medicine, People’s Hospital of Ningxia Hui Autonomous Region, Yinchuan, People’s Republic of China; 2Department of Respiratory Medicine, First Affiliated Hospital of Northwest Minzu University, Yinchuan, People’s Republic of China; 3Department of Intervention and Vascular Surgery, People’s Hospital of Ningxia Hui Autonomous, Yinchuan, People’s Republic of China; 4Department of Intervention and Vascular Surgery, First Affiliated Hospital of Northwest Minzu University, Yinchuan, People’s Republic of China*These authors contributed equally to this workCorrespondence: Bing ZhuanDepartment of Respiratory Medicine, First Affiliated Hospital of Northwest Minzu University, No. 301 Zhengyuan North Street, Jinfeng District, Yinchuan, 750004, People’s Republic of ChinaTel +86 18709518179Email Zhuanb518@163.comPurpose: Lung cancer represents one of the most frequent solid tumors. Adenocarcinoma is a common type of tumor and a significant threat to individual health globally. MicroRNAs (miRNAs) are recognized as critical governors of gene expression during carcinogenesis, while their effects on lung cancer occurrence and development are required for further investigation. Herein, the functional role of miR-210-3p and its regulation mechanism were characterized in lung cancer.Methods: A total of 50 pairs of tumor and tumor-free lung tissues were surgically resected from lung cancer patients. Dual-luciferase reporter assay and RNA immunoprecipitation assay were performed to examine USF1 binding with miR-210-3p and PCGF3. Cultured human lung cancer cells A549 were assayed for viability, apoptosis, migration, and invasion in vitro by CCK-8 test, flow cytometry, transwell chamber assays, tumorigenesis, and lymph node metastasis in vivo by mouse xenograft experiments.Results: miR-210-3p was upregulated in lung cancer tissues. The inhibition of miR-210-3p by specific inhibitor tempered lung cancer development and metastasis in vitro and in vivo. miR-210-3p targeted USF1 and inhibited its expression. USF1 was bound with PCGF3, which increased its transcription. PCGF3-specific knockdown mimicked the effect of miR-210-3p on lung cancer development and metastasis in vitro and in vivo.Conclusion: The current study demonstrated that miR-210-3p facilitates lung cancer development and metastasis by impairing USF1-mediated promotion of PCGF3, which provides a better understanding of the mechanism of lung cancer development and metastasis.Keywords: lung cancer, miR-210-3p, USF1, PCGF3
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