Background: NudC domain containing 1 (NudCD1) is an oncoprotein related to diverse cancers. This study aims to investigate the expression, role, and regulatory mechanism of NudCD1 in non-small cell lung cancer (NSCLC). Methods: qRT-PCR, Western blot, and immunohistochemistry were performed to detect the expressions of NudCD1 in NSCLC tissues and cell lines. The correlation between NudCD1 expression and clinical features was determined by the χ2 test. Besides, shRNA was used to construct the NudCD1 low expression model of NCI-H1299 and NCI-H460 cells, and CCK-8 and transwell assay were conducted to monitor the changes of proliferation, migration, and invasion of cancer cells. The expression levels of epithelial-mesenchymal transition markers and IGF1R-ERK1/2 signaling pathway proteins were detected by Western blot. Results: The expression of NudCD1 in NSCLC was higher than that in normal tissues, and the increased expression of NudCD1 was significantly correlated with increased T stage and lymph node metastasis. Moreover, patients with high expression of NudCD1 had worse prognosis. NudCD1 knockdown was proven to impede the proliferation but facilitate the migration and invasion of cancer cells. Furthermore, knockdown of NudCD1 resulted in an increase in the expression of E-cadherin and a decrease in the expression of vimentin. We also observed that NudCD1 overexpression promoted the phosphorylation of IGF1R and ERK1/2 proteins. Conclusion: NudCD1 promotes the proliferation and metastasis of NSCLC cells via activation of IGF1R-ERK1/2, which indicates that NudCD1 may be a potential therapy target of NSCLC.

中文翻译：

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NudCD1通过激活IGF1R-ERK1/2促进非小细胞肺癌细胞的增殖和转移

背景：含有 1 的 NudC 结构域 (NudCD1) 是一种与多种癌症相关的癌蛋白。本研究旨在探讨NudCD1在非小细胞肺癌（NSCLC）中的表达、作用和调控机制。方法：采用qRT-PCR、Western blot、免疫组化等方法检测NudCD1在NSCLC组织和细胞系中的表达。NudCD1 表达与临床特征之间的相关性通过 χ2 检验确定。此外，利用shRNA构建NCI-H1299和NCI-H460细胞NudCD1低表达模型，并通过CCK-8和transwell实验监测癌细胞增殖、迁移和侵袭的变化。Western blot检测上皮间质转化标志物和IGF1R-ERK1/2信号通路蛋白的表达水平。结果：NudCD1在NSCLC中的表达高于正常组织，NudCD1的表达增加与T分期增加和淋巴结转移显着相关。此外，NudCD1高表达的患者预后较差。NudCD1 敲低被证明会阻碍癌细胞的增殖，但会促进癌细胞的迁移和侵袭。此外，NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1的表达增加与T分期和淋巴结转移显着相关。此外，NudCD1高表达的患者预后较差。NudCD1 敲低被证明会阻碍癌细胞的增殖，但会促进癌细胞的迁移和侵袭。此外，NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1的表达增加与T分期和淋巴结转移显着相关。此外，NudCD1高表达的患者预后较差。NudCD1 敲低被证明会阻碍癌细胞的增殖，但会促进癌细胞的迁移和侵袭。此外，NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1高表达的患者预后较差。NudCD1 敲低被证明会阻碍癌细胞的增殖，但会促进癌细胞的迁移和侵袭。此外，NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1高表达的患者预后较差。NudCD1 敲低被证明会阻碍癌细胞的增殖，但会促进癌细胞的迁移和侵袭。此外，NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。NudCD1 的敲低导致 E-cadherin 表达增加和波形蛋白表达减少。我们还观察到 NudCD1 过表达促进了 IGF1R 和 ERK1/2 蛋白的磷酸化。结论：NudCD1通过激活IGF1R-ERK1/2促进NSCLC细胞的增殖和转移，表明NudCD1可能是NSCLC的潜在治疗靶点。