Lung cancer is the leading cause of cancer‐related death worldwide. Previous studies revealed that endoplasmic reticulum oxidoreductase 1 alpha (ERO1L) played critical roles in the malignant behaviors of several cancer types, but its role in non‐small cell lung cancer (NSCLC) remained unclear. In this study, we identified 26 upregulated and 102 downregulated genes in NSCLC using bioinformatics analyses, and these genes were enriched in the biological processes of the cell cycle. ERO1L was remarkably upregulated in NSCLC and overexpression of ERO1L was associated with poor prognosis of NSCLC. ERO1L deficiency markedly suppressed NSCLC cell proliferation, colony formation, migration, and invasion. ERO1L depletion caused a dramatically decreased expression of cell cycle‐related factors in NSCLC cells. Collectively, our data validated that ERO1L could function as a tumor promoter in NSCLC, indicating the potential of targeting ERO1L for the treatment of NSCLC.

中文翻译：

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ERO1L通过调节细胞周期相关分子来促进NSCLC的发展。

肺癌是全球癌症相关死亡的主要原因。先前的研究表明，内质网氧化还原酶1α（ERO1L）在几种癌症类型的恶性行为中起关键作用，但其在非小细胞肺癌（NSCLC）中的作用仍不清楚。在这项研究中，我们使用生物信息学分析鉴定了NSCLC中的26个上调基因和102个下调基因，这些基因在细胞周期的生物学过程中富集。ERO1L在NSCLC中显着上调，而ERO1L的过表达与NSCLC的预后不良有关。ERO1L缺乏明显抑制NSCLC细胞增殖，集落形成，迁移和侵袭。ERO1L耗竭导致NSCLC细胞中细胞周期相关因子的表达急剧下降。总的来说，