Downregulated microRNA‑140‑5p expression regulates apoptosis, migration and invasion of lung cancer cells by targeting zinc finger protein 800
- Enqing Zhuo
- Changqing Cai
- Wenzhe Liu
- Kunsong Li
- Wenzhen Zhao
Affiliations: Department of 2nd Oncology, Guangdong Second Provincial General Hospital, Guangzhou, Guangdong 510317, P.R. China
- Published online on: October 29, 2020 https://doi.org/10.3892/ol.2020.12253
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Despite advances in the diagnosis and treatment in recent years, lung cancer is still one of the primary causes of cancer‑associated morbidity and mortality in globally. Abnormally expressed microRNAs (miRNAs/miRs) in tumor tissues serve vital roles in the pathological mechanism of tumors and have become prospective biomarkers for cancer diagnosis. The present study aimed to investigate the effects of the miR‑140‑5p/zinc finger protein 800 (ZNF800) axis in lung carcinoma, and determine its potential underlying molecular mechanisms. The degree of cell proliferation was assessed via the MTT assay, while the migratory and invasive abilities of lung cancer cells were determined via the Transwell and Matrigel assays. The expression levels of miR‑140‑5p and ZNF800 were detected via reverse transcription‑quantitative PCR and western blot analyses. The results demonstrated that miR‑140‑5p expression was notably higher in normal human bronchial epithelial cells compared with the respective lung cancer cell lines, H292, PC‑9, CL1‑5 and H460. Furthermore, miR‑140‑5p expression increased in the lung cancer cells compared with the control cells following transfection with miR‑140‑5p mimic. Overexpressing miR‑140‑5p significantly suppressed the proliferative, invasive and migratory abilities of H460 and PC‑9 cells, and stimulated cell apoptosis by upregulating the expression of cleaved‑caspase‑3. Notably, these effects were reversed following transfection with miR‑140‑5p inhibitor. miR‑140‑5p was predicted as a negative regulator of ZNF800, and ZNF800 knockdown significantly suppressed the proliferative and metastatic abilities of lung adenocarcinoma (LUAD) cells, which was comparable to the effects of miR‑140‑5p mimic. Taken together, these results suggest that miR‑140‑5p may block the malignant phenotype of LUAD by negatively regulating ZNF800 expression. Thus, the miR‑140‑5p/ZNF800 axis may be used as an alternative therapeutic target for lung carcinoma in general, and LUAD in particular.