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

hsa_circ_0077837通过调控miR-1178-3p/APITD1轴减轻非小细胞肺癌的恶性程度

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作者:Shanlin Xu, Yanyan Jiang, Yaqian Duan

Conclusion

Collectively, our findings validated that hsa_circ_0077837 served as a miR-1178-3p sponge by targeting APITD1 that alleviated 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.

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.

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.

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