Non-small cell lung cancer (NSCLC) is one of the most common malignant tumors worldwide. Circular RNAs (circRNAs) have been widely reported to play a role in the pathogenesis of various tumors. Nevertheless, the function of circ_0001955 in NSCLC progression has not been explored yet. This study aims to explore the functions of circ_0001955 in NSCLC and investigate its regulatory molecular mechanism. First, we determined that circ_0001955 was upregulated in NSCLC cells. Subsequently, we demonstrated that knockdown of circ_0001955 restrained cell proliferation and invasion. In vivo experiments further proved the suppressive effect of circ_0001955 silence on tumor growth. Mechanism assays revealed that circ_0001955 enhanced nuclear factor-κB (NF-κB) inhibitor interacting Ras-like protein 2 (NKIRAS2) expression by sponging microRNA-29a-3p (miR-29a-3p). Upregulation of NKIRAS2 led to the deceased level of IκBβ but increased levels of nuclear p65, thus activating the NF-κB signaling pathway. In conclusion, Circ_0001955 activates the NF-κB pathway to promote NSCLC cell proliferation and invasion by regulating miR-29a-3p/NKIRAS2 axis.

中文翻译：

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Circ_0001955通过调节MiR-29a-3p/NKIRAS2轴激活核因子-κB通路促进非小细胞肺癌细胞增殖和侵袭

非小细胞肺癌（NSCLC）是全球最常见的恶性肿瘤之一。环状RNA（circRNA）已被广泛报道在各种肿瘤的发病机制中发挥作用。然而，circ_0001955在NSCLC进展中的功能尚未被探索。本研究旨在探讨circ_0001955在NSCLC中的功能并探讨其调控分子机制。首先，我们确定 circ_0001955 在 NSCLC 细胞中上调。随后，我们证明了circ_0001955的敲除抑制了细胞增殖和侵袭。体内实验进一步证明了circ_0001955沉默对肿瘤生长的抑制作用。机制分析显示，circ_0001955 通过海绵 microRNA-29a-3p (miR-29a-3p) 增强核因子-κB (NF-κB) 抑制剂相互作用 Ras 样蛋白 2 (NKIRAS2) 的表达。NKIRAS2的上调导致IκBβ水平降低，但核p65水平升高，从而激活NF-κB信号通路。总之，Circ_0001955通过调节miR-29a-3p/NKIRAS2轴激活NF-κB通路促进NSCLC细胞增殖和侵袭。