PDZ and LIM domain containing protein 2 (PDLIM2) has been identified as a vital tumor-associated gene that is aberrantly expressed in various types of tumors. Yet, the involvement of PDLIM2 in non-small cell lung cancer (NSCLC) is currently undetermined. The design of the current study was to evaluate whether PDLIM2 plays a role in NSCLC. We found that PDLIM2 expression was commonly decreased in NSCLC tissues. Moreover, low expression of PDLIM2 was also detected in NSCLC cell lines and demethylation treatment restored PDLIM2 expression. The re-expression of PDLIM2 impeded the proliferative, colony-forming, and invasive capabilities of NCLCL cells. In contrast, depletion of PDLIM2 markedly enhanced the malignant behaviors of NSCLC cells. Notably, PDLIM2 overexpression downregulated the expression of nuclear factor (NF)-κB p65 subunit and repressed NF-κB transcription reporter activity in NSCLC cells. The overexpression of p65 significantly reversed PDLIM2-mediated antitumor effects in NSCLC cells. Additionally, the Xenograft tumor formation assay revealed that the overexpression of PDLIM2 markedly restricted the tumor growth of NSCLC in vivo. Overall, our study confirms that PDLIM2 acts as a tumor-inhibitor in NSCLC through the inactivation of NF-κB, suggesting PDLIM2 as a candidate therapeutic target for NSCLC.

含PDZ和LIM域的蛋白2（PDLIM2）已被确定为重要的肿瘤相关基因，在各种类型的肿瘤中异常表达。然而，目前尚不确定PDLIM2是否参与非小细胞肺癌（NSCLC）。本研究的设计旨在评估PDLIM2是否在NSCLC中发挥作用。我们发现NSCLC组织中PDLIM2表达通常降低。而且，在NSCLC细胞系中也检测到PDLIM2的低表达，并且去甲基化处理恢复了PDLIM2的表达。PDLIM2的重新表达阻碍了NCLCL细胞的增殖，集落形成和侵袭能力。相反，PDLIM2的消耗显着增强了NSCLC细胞的恶性行为。值得注意的是 PDLIM2过表达下调了NSCLC细胞中核因子（NF）-κBp65亚基的表达，并抑制了NF-κB转录报告基因的活性。p65的过表达显着逆转了NSCLC细胞中PDLIM2介导的抗肿瘤作用。此外，异种移植肿瘤形成试验表明，PDLIM2的过表达显着限制了NSCLC的肿瘤生长体内。总体而言，我们的研究证实PDLIM2通过NF-κB的失活而在NSCLC中起着肿瘤抑制剂的作用，这表明PDLIM2是NSCLC的候选治疗靶点。