肺癌是世界上第二大常见癌症，死亡率最高。 Calumenin 作为分子伴侣，不仅结合内质网内的各种蛋白质，而且在与肿瘤发展相关的多种过程中发挥着至关重要的作用。然而，钙蛋白在肺腺癌中的调节机制仍不清楚。在此，我们研究了calumenin对肺腺癌的影响并探讨了可能的机制。通过5-乙炔基-2'-脱氧尿苷测定、集落形成、Transwell和伤口愈合实验来探讨calumenin对肺腺癌增殖和迁移的影响细胞。为了深入了解calumenin敲低抑制肺腺癌迁移和增殖的潜在机制，我们通过比较calumenin敲低与正常A549，进行了基于转录组学的基因本体论、京都基因和基因组百科全书、基因集富集分析和独创性通路分析calumenin在肺腺癌中的mRNA和蛋白水平高表达，与该疾病的不良预后相关。 Calumenin 增强 A549 和 H1299 细胞的增殖和迁移。基因集富集分析显示，A549 细胞中 calumenin 的敲低显着抑制 MYC 和 V-Ki-ras2 Kirsten 大鼠肉瘤病毒癌基因同源信号通路，同时激活干扰素信号、炎症信号和 p53 通路。 Ingenuity通路分析提供了额外的见解，表明A549细胞中calumenin敲低后干扰素和炎症通路显着激活。calumenin敲低的抗癌机制可能与MYC和KRAS信号的抑制有关，但与干扰素信号的激活有关，炎症信号和 p53 通路。© 2024。作者。

Lung cancer is the second most common cancer with the highest mortality in the world. Calumenin as a molecular chaperone that not only binds various proteins within the endoplasmic reticulum but also plays crucial roles in diverse processes associated with tumor development. However, the regulatory mechanism of calumenin in lung adenocarcinoma remains elusive. Here, we studied the impact of calumenin on lung adenocarcinoma and explored possible mechanisms.5-ethynyl-2'-deoxyuridine assay, colony formation, transwell and wound healing assays were performed to explore the effects of calumenin on the proliferation and migration of lung adenocarcinoma cells. To gain insights into the underlying mechanisms through which calumenin knockdown inhibits the migration and proliferation of lung adenocarcinoma, we performed Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis and Ingenuity Pathway Analysis based on transcriptomics by comparing calumenin knockdown with normal A549 cells.The mRNA and protein levels of calumenin in lung adenocarcinoma are highly expressed and they are related to an unfavorable prognosis in this disease. Calumenin enhances the proliferation and migration of A549 and H1299 cells. Gene Set Enrichment Analysis revealed that knockdown of calumenin in A549 cells significantly inhibited MYC and V-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog signaling pathways while activating interferon signals, inflammatory signals, and p53 pathways. Ingenuity pathway analysis provided additional insights, indicating that the interferon and inflammatory pathways were prominently activated upon calumenin knockdown in A549 cells.The anti-cancer mechanism of calumenin knockdown might be related to the inhibition of MYC and KRAS signals but the activation of interferon signals, inflammatory signals and p53 pathways.© 2024. The Author(s).