c-MYC在调节淋巴造血和促进淋巴瘤形成中的重要性已经得到充分证实，但其亲属MNT在支持作用方面的重要性却鲜为人知。利用Rag1Cre介导的淋巴祖细胞中的Mnt删除，我们在这里表明，在正常T细胞发育过程中，MNT损失会增强细胞凋亡，至少部分原因是通过升高凋亡诱导蛋白BIM的表达。此外，利用易患T淋巴瘤的VavP-MYC转基因小鼠，我们发现Mnt的删除减少了MYC驱动的预恶性T淋巴细胞群，并消除了胸腺T淋巴瘤。此外，我们证实Mnt的删除可以预防γ-辐射小鼠中的T淋巴瘤发展，很可能是通过增强再生 depleted thymus的T淋巴细胞的细胞凋亡而实现的。结合我们最近的研究，即MNT对于MYC驱动的预恶性和恶性B淋巴细胞的生存至关重要，这些结果表明MNT代表着新的重要药物靶点，适用于T和B淋巴细胞恶性肿瘤。©2023年作者。

The importance of c-MYC in regulating lymphopoiesis and promoting lymphomagenesis is well-established. Far less appreciated is the vital supporting role of MYC's relative MNT. Using Rag1Cre-mediated Mnt deletion in lymphoid progenitor cells, we show here that, during normal T cell development, MNT loss enhances apoptosis, at least in part by elevating expression of the pro-apoptotic BH3-only protein BIM. Moreover, using T lymphoma-prone VavP-MYC transgenic mice, we show that Mnt deletion reduces the pool of pre-malignant MYC-driven T lymphoid cells and abrogates thymic T lymphomagenesis. In addition, we establish that Mnt deletion prevents T lymphoma development in γ-irradiated mice, most likely by enhancing apoptosis of T lymphoid cells repopulating the depleted thymus. Taken together with our recent demonstration that MNT is vital for the survival of MYC-driven pre-malignant and malignant B lymphoid cells, these results suggest that MNT represents an important new drug target for both T and B lymphoid malignancies.© 2023. The Author(s).