据报道，肿瘤坏死因子 α 诱导蛋白 3 (TNFAIP3) 对各种癌症的自噬调节具有重要意义。本研究旨在通过调节自噬来解读 TNFAIP3 在弥漫性大 B 细胞淋巴瘤 (DLBCL) 中的作用和机制。有关 TNFAIP3 在 DLBCL 中的差异表达和预后作用的信息来自基因表达综合 (GEO) 数据库。通过实时定量聚合酶链反应（qRT-PCR）和Western blotting检测人DLBCL细胞中TNFAIP3的表达水平。采用细胞计数试剂盒 8 (CCK-8) 和集落形成测定来测定细胞增殖。 Transwell实验和流式细胞术分别检测细胞迁移和凋亡。使用免疫荧光和透射电镜评估细胞自噬。凋亡标志物（caspase-3、cleaved-caspase-3、Bcl-2 Associated X（Bax）、B细胞淋巴瘤-2（Bcl-2））水平、自噬指标（微管相关蛋白1A/的比例） 1B 轻链 3 II 和 I (LC3II/LC3I)、Sequestosome (p62)) 和通路蛋白（Toll 样受体 4 (TLR4)、骨髓分化初级反应 88 (MyD88)、转录因子 NF-Kappa-B P65 亚基(p65) 和磷酸化 p65 (p-p65)) 通过蛋白质印迹进行评估。采用免疫组织化学法检测肿瘤组织中Ki67的表达。DLBCL样本中TNFAIP3表达下调，与不良预后相关。 DLBCL 细胞中 TNFAIP3 表达也下调。结果发现TNFAIP3阻碍细胞增殖和迁移，并增强OCI-LY3细胞的凋亡。自噬抑制剂3-甲基腺嘌呤（3-MA）的干预显着逆转了TNFAIP3诱导的OCI-LY3细胞凋亡。此外，TNFAIP3通过调节TLR4/MyD88/核因子κB（NF-κB）信号通路诱导自噬。体内实验表明，DLBCL中TNFAIP3表达下调，上调TNFAIP3可抑制肿瘤生长。TNFAIP3通过诱导TLR4/MyD88/NF-κB通路介导的自噬抑制DLBCL进展。

Tumor necrosis factor alpha induced protein 3 (TNFAIP3) is reportedly to have significant implications for autophagy regulation in various cancers. The current study aimed to decipher the role and mechanism of TNFAIP3 in diffuse large B-cell lymphoma (DLBCL) by modulating autophagy.Information pertaining to the differential expression and prognostic role of TNFAIP3 in DLBCL was gleaned from the Gene Expression Omnibus (GEO) database. The TNFAIP3 expression levels in human DLBCL cells were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. Cell counting kit-8 (CCK-8) and colony formation assays were employed to determine cell proliferation. Transwell assay and flow cytometry were applied to detect cell migration and apoptosis, respectively. Immunofluorescence and transmission electron microscope were used for the assessment of cell autophagy. The levels of apoptotic markers (caspase-3, cleaved-caspase-3, Bcl-2 Associated X (Bax), and B cell lymphoma-2 (Bcl-2)), autophagy indicators (the ratio of microtubule-associated proteins 1A/1B light chain 3 II and I (LC3II/LC3I), Sequestosome (p62)), and pathway proteins (toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), Transcription Factor NF-Kappa-B P65 Subunit (p65), and phosphorylated-p65 (p-p65)) were assessed via Western blotting. Immunohistochemistry was employed to detect Ki67 expression in tumor tissues.TNFAIP3 expression in DLBCL samples was downregulated, correlating with poor prognosis. TNFAIP3 expression was also downregulated in DLBCL cells. It was found that TNFAIP3 impeded cell proliferation and migration, and enhanced apoptosis of OCI-LY3 cells. Intervention with autophagy inhibitor 3-methyladenine (3-MA) markedly reversed apoptosis of OCI-LY3 cells induced by TNFAIP3. Besides, TNFAIP3 induced autophagy via modulating the TLR4/MyD88/nuclear factor kappa B (NF-κB) signaling pathway. In vivo experiments showed that TNFAIP3 expression in DLBCL was downregulated, and upregulation of TNFAIP3 could inhibit tumor growth.TNFAIP3 inhibits DLBCL progression by inducing TLR4/MyD88/NF-κB pathway-mediated autophagy.