Non-small-cell lung cancer (NSCLC) is one of the most common solid tumors and the leading cause of lung cancer-related fatality. Growing evidence has indicated that circular RNAs (circRNAs) play important roles in the progression of multiple human cancers. As a novel circRNA, very little research has focused on the function of circRNA TUBA1C (circTUBA1C) in cancer development, including NSCLC. In the present study, we found that the expression of circTUBA1C was significantly upregulated in NSCLC tissues. The loss-of function assays suggested that circTUBA1C deficiency notably hampered cell proliferation as well as accelerated cell apoptosis in NSCLC. In mechanism, we discovered that circTUBA1C could act as a sponge for miR-143-3p and then negatively regulate miR-143-3p. Moreover, rescue assays demonstrated that knockdown of miR-143-3p could reverse circTUBA1C silence-mediated effects on cell proliferation and apoptosis. Besides, we established a xenografted tumor model to investigate the function of circTUBA1C in vivo. The result illustrated that the decline of tumor growth resulted from circTUBA1C deficiency could be recovered by miR-143-3p knockdown. Taken together, these findings indicated the important role of circTUBA1C/miR-143-3p axis in NSCLC, which may provide a potential target for NSCLC therapy.

非小细胞肺癌 (NSCLC) 是最常见的实体瘤之一，也是肺癌相关死亡的主要原因。越来越多的证据表明，环状 RNA（circRNA）在多种人类癌症的进展中发挥着重要作用。作为一种新型 circRNA，很少有研究关注 circRNA TUBA1C (circTUBA1C) 在癌症发展中的功能，包括 NSCLC。在本研究中，我们发现 circTUBA1C 在 NSCLC 组织中的表达显着上调。功能丧失分析表明，circTUBA1C 缺陷显着阻碍了 NSCLC 中的细胞增殖以及加速细胞凋亡。在机制上，我们发现circTUBA1C可以充当miR-143-3p的海绵，然后负调控miR-143-3p。而且，救援分析表明，敲除 miR-143-3p 可以逆转 circTUBA1C 沉默介导的细胞增殖和凋亡作用。此外，我们建立了异种移植肿瘤模型来研究 circTUBA1C 在体内 的功能。结果表明，由于 circTUBA1C 缺陷导致的肿瘤生长下降可以通过敲低 miR-143-3p 来恢复。总之，这些发现表明 circTUBA1C/miR-143-3p 轴在 NSCLC 中的重要作用，这可能为 NSCLC 治疗提供一个潜在的靶点。