这项研究揭示了癌蛋白 DEK 在 B 细胞淋巴瘤中的关键作用。我们发现，在诊断为低级别 B 细胞淋巴瘤 (LGBCL) 的病例中，DEK 表达与肿瘤增殖增加和总体生存率较差相关。我们还发现 LGBCL 肿瘤中 DEK 表达与拷贝数改变之间存在显着相关性，这凸显了 LGBCL 发病机制的一个新机制，值得进一步探索。为了探究 DEK 在 B 细胞淋巴瘤中的机制作用，我们构建了 DEK 敲除细胞系模型，该模型证明 DEK 耗竭导致增殖减少以及关键细胞周期和凋亡相关蛋白（包括 Bcl-2、Bcl-xL）表达的改变和 p53。值得注意的是，DEK 耗尽的细胞对细胞凋亡诱导剂（包括 Venetoclax 和 staurosporine）表现出更高的敏感性，这强调了靶向 DEK 在 B 细胞淋巴瘤中的治疗潜力。总体而言，我们的研究有助于更好地了解 DEK 作为 B 细胞淋巴瘤中癌蛋白的作用，强调其作为有前途的治疗靶点和侵袭性 LGBCL 的新型生物标志物的潜力。进一步的研究阐明 DEK 介导的肿瘤发生的分子机制可以为改善 B 细胞淋巴瘤患者的治疗策略和更好的临床结果铺平道路。© 2024。作者。

This study sheds light on the pivotal role of the oncoprotein DEK in B-cell lymphoma. We reveal DEK expression correlates with increased tumor proliferation and inferior overall survival in cases diagnosed with low-grade B-cell lymphoma (LGBCL). We also found significant correlation between DEK expression and copy number alterations in LGBCL tumors, highlighting a novel mechanism of LGBCL pathogenesis that warrants additional exploration. To interrogate the mechanistic role of DEK in B-cell lymphoma, we generated a DEK knockout cell line model, which demonstrated DEK depletion caused reduced proliferation and altered expression of key cell cycle and apoptosis-related proteins, including Bcl-2, Bcl-xL, and p53. Notably, DEK depleted cells showed increased sensitivity to apoptosis-inducing agents, including venetoclax and staurosporine, which underscores the therapeutic potential of targeting DEK in B-cell lymphomas. Overall, our study contributes to a better understanding of DEK's role as an oncoprotein in B-cell lymphomas, highlighting its potential as both a promising therapeutic target and a novel biomarker for aggressive LGBCL. Further research elucidating the molecular mechanisms underlying DEK-mediated tumorigenesis could pave the way for improved treatment strategies and better clinical outcomes for patients with B-cell lymphoma.© 2024. The Author(s).