Lung carcinoma (LC) is a complicated and highly heterogeneous disease with high morbidity and mortality. Both lysyl oxidase-like (LOXL) 2 and 3 act in cancer progression. This work endeavors to illustrate the influence of LOXL2/LOXL3 on LC progression and the underlying mechanisms. LOXL family genes and CCAAT enhancer binding protein A (CEBPA) were analyzed in the TCGA database for their expression patterns in LC patients and their correlations with the patient's prognosis. CEBPA, LOXL2, and LOXL3 expression levels were determined in LC cells. Gain- and loss-of-function assays were conducted, followed by assays for cell proliferation, epithelial-mesenchymal transition (EMT), apoptosis, invasion, and migration. The binding of CEBPA or B cell lymphoma protein (BCL)-2 to LOXL2/LOXL3 was verified. The ubiquitination level of BCL-2 and histone acetylation level of LOXL2/LOXL3 in LC cells were analyzed. Database analyses revealed that LC patients had high CEBPA, LOXL2, and LOXL3 expression, which were related to poor prognosis. LC cells also exhibited high CEBPA, LOXL2, and LOXL3 levels. LOXL2/LOXL3 knockdown subdued EMT, proliferation, migration, and invasion while enhancing the apoptosis of LC cells. LOXL2/LOXL3 could bind to CEBPA and BCL-2. LOXL2/LOXL3 knockdown upregulated BCL-2 ubiquitination level and diminished BCL-2 expression in LC cells. CEBPA recruited Tip60 to enhance histone acetylation and transcription of LOXL2/LOXL3 in LC cells. BCL-2 overexpression abolished the impacts of LOXL2/LOXL3 knockdown on LC cells. In conclusion, CEBPA boosts LOXL2 and LOXL3 transcription to facilitate BCL-2 stability by recruiting Tip60 and thus contributes to LC cell growth and metastasis.

肺癌（LC）是一种复杂且高度异质性的疾病，具有高发病率和死亡率。赖氨酰氧化酶样 (LOXL) 2 和 3 均在癌症进展中发挥作用。这项工作致力于阐明 LOXL2/LOXL3 对 LC 进展的影响及其潜在机制。在 TCGA 数据库中分析了 LOXL 家族基因和 CCAAT 增强子结合蛋白 A (CEBPA) 在 LC 患者中的表达模式及其与患者预后的相关性。测定 LC 细胞中的 CEBPA、LOXL2 和 LOXL3 表达水平。进行功能获得和功能丧失测定，然后进行细胞增殖、上皮间质转化（EMT）、细胞凋亡、侵袭和迁移的测定。验证了 CEBPA 或 B 细胞淋巴瘤蛋白 (BCL)-2 与 LOXL2/LOXL3 的结合。分析LC细胞中BCL-2的泛素化水平和LOXL2/LOXL3的组蛋白乙酰化水平。数据库分析显示，LC患者CEBPA、LOXL2和LOXL3高表达，这与预后不良有关。LC 细胞还表现出高 CEBPA、LOXL2 和 LOXL3 水平。LOXL2/LOXL3 敲低可抑制 EMT、增殖、迁移和侵袭，同时增强 LC 细胞的凋亡。LOXL2/LOXL3可以结合CEBPA和BCL-2。LOXL2/LOXL3 敲除上调 BCL-2 泛素化水平并减少 LC 细胞中的 BCL-2 表达。CEBPA 招募 Tip60 来增强 LC 细胞中 LOXL2/LOXL3 的组蛋白乙酰化和转录。BCL-2 过表达消除了 LOXL2/LOXL3 敲低对 LC 细胞的影响。总之，CEBPA 通过招募 Tip60 增强 LOXL2 和 LOXL3 转录，以促进 BCL-2 稳定性，从而有助于 LC 细胞生长和转移。