Non-small cell lung cancer (NSCLC) is the most common type of lung cancer. Although significant advances have been achieved in the treatment of NSCLC during the past two decades, the 5-year survival rate of patients with NSCLC remains <20%. Thus, there is an urgent requirement to further understand the molecular mechanisms that promote NSCLC development and to identify novel therapeutic targets. In the present study, the gene expression profiles of patients with NSCLC from The Cancer Genome Atlas database were carefully analyzed and SPINK1 was identified as a tumor-inducing factor. SPINK1 expression level was found to be increased in both NSCLC tissues and cell lines. Moreover, SPINK1 promoted cell proliferation in A549 and H1299 cells. Knockdown of SPINK1 could activate cell autophagy and apoptosis. Mechanistically, SPINK1 was demonstrated to induce the proliferation of NSCLC via activating the MEK/ERK signaling pathway. In conclusion, these findings suggested that SPINK1 may serve as a potential biomarker in NSCLC.

非小细胞肺癌（NSCLC）是最常见的肺癌类型。尽管在过去的二十年中，NSCLC 的治疗取得了重大进展，但 NSCLC 患者的 5 年生存率仍低于 20%。因此，迫切需要进一步了解促进NSCLC发展的分子机制并确定新的治疗靶点。在本研究中，对来自癌症基因组图谱数据库的 NSCLC 患者的基因表达谱进行了仔细分析，并将 SPINK1 确定为肿瘤诱导因子。发现 SPINK1 表达水平在 NSCLC 组织和细胞系中均增加。此外，SPINK1 促进 A549 和 H1299 细胞的细胞增殖。SPINK1 的敲低可激活细胞自噬和凋亡。机械地，SPINK1 被证明通过激活 MEK/ERK 信号通路诱导 NSCLC 的增殖。总之，这些发现表明 SPINK1 可能作为 NSCLC 中的潜在生物标志物。