hsa_circ_0077837 Alleviated the Malignancy of Non-Small Cell Lung Cancer by Regulating the miR-1178-3p/APITD1 Axis

Author:

Xu Shanlin1ORCID,Jiang Yanyan2ORCID,Duan Yaqian3ORCID

Affiliation:

1. Department of Oncology, Zibo Central Hospital, Zibo, Shandong 255000, China

2. Department of Respiration, Zibo Central Hospital, Zibo, Shandong 255000, China

3. Department of Respiratory and Critical Care Medicine, Shandong Province Chest Hospital, Jinan, Shandong 250000, China

Abstract

Objective. circRNAs were a group of the most promising molecular biomarkers for clinical prognosis and diagnosis of non-small cell lung cancer (NSCLC). It was a pity that academic circle still struggled to figure out how circRNAs acted on NSCLC. This article aimed to study the function and mechanism of hsa_circ_0077837 in NSCLC progression. Methods. Cell viability was measured via CCK-8, while apoptosis was evaluated with flow cytometry. The transwell assay and scratch test were used to detect invasion and migration, respectively. The dual-luciferase reporter gene assay verified the regulatory effect of miR-1178-3p on hsa_circ_0077837 and miR-1178-3p on apoptosis-inducing, TAF9-like domain 1 (APITD1). The TUNEL assay and immunohistochemistry were used to assess cells apoptosis and proliferation in lung tumor tissues in mice. Results. Hsa_circ_0077837 and APITD1 expression were suppressed in NSCLC tissues and cells, and miR-1178-3p level was promoted. High amount of hsa_circ_0077837 intensely prevented cell proliferation, migration, and invasion, promoted cell apoptosis in vitro, and delayed tumor growth in mice. Further analysis indicated that hsa_circ_0077837 acted as a miR-1178-3p sponge to stabilize APITD1, the target of miR-1178-3p. Mechanistically, we discovered that hsa_circ_0077837 could prevent proliferation, viability, migration, and invasion of NSCLC cells through stimulating the miR-1178-3p/APITD1 pathway. Conclusion. Collectively, our findings validated that hsa_circ_0077837 served as a miR-1178-3p sponge by targeting APITD1 that alleviated NSCLC progression.

Funder

Jiangsu University

Publisher

Hindawi Limited

Subject

Oncology

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