Xu Shanlin, Jiang Yanyan, Duan Yaqian
Department of Oncology, Zibo Central Hospital, Zibo, Shandong 255000, China.
Department of Respiration, Zibo Central Hospital, Zibo, Shandong 255000, China.
J Oncol. 2022 Mar 9;2022:3902832. doi: 10.1155/2022/3902832. eCollection 2022.
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.
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.
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 , 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.
Collectively, our findings validated that hsa_circ_0077837 served as a miR-1178-3p sponge by targeting APITD1 that alleviated NSCLC progression.
环状RNA(circRNAs)是一组对非小细胞肺癌(NSCLC)临床预后和诊断最具潜力的分子生物标志物。遗憾的是,学术界仍在努力弄清楚circRNAs如何作用于NSCLC。本文旨在研究hsa_circ_0077837在NSCLC进展中的功能和机制。
通过CCK-8检测细胞活力,采用流式细胞术评估细胞凋亡。分别用Transwell实验和划痕实验检测侵袭和迁移能力。双荧光素酶报告基因实验验证miR-1178-3p对hsa_circ_0077837的调控作用以及miR-1178-3p对凋亡诱导TAF9样结构域1(APITD1)的调控作用。采用TUNEL实验和免疫组化评估小鼠肺肿瘤组织中的细胞凋亡和增殖情况。
hsa_circ_0077837和APITD1在NSCLC组织和细胞中的表达受到抑制,而miR-1178-3p水平升高。高表达的hsa_circ_0077837强烈抑制细胞增殖、迁移和侵袭,促进细胞凋亡,并延缓小鼠肿瘤生长。进一步分析表明,hsa_circ_0077837作为miR-1178-3p的海绵,稳定miR-1178-3p的靶标APITD1。机制上,我们发现hsa_circ_0077837可通过激活miR-1178-3p/APITD1通路抑制NSCLC细胞的增殖、活力、迁移和侵袭。
总体而言,我们的研究结果证实hsa_circ_0077837作为miR-1178-3p的海绵,靶向APITD1,从而缓解NSCLC进展。