Abstract：
N-acetyltransferase 10 (NAT10), a versatile enzyme, has gained considerable attention as a significant player in the complex realm of cancer biology. Its enigmatic role in tumorigenesis extends across a wide array of cellular processes, impacting cell growth, differentiation, survival, and genomic stability. Within the intricate network of oncogenic signaling, NAT10 emerges as a crucial agent in multiple cancer types, such as breast, lung, colorectal, and leukemia. This compelling research addresses the intricate complexity of the mechanistic role of NAT10 in cancer development. By elucidating its active participation in essential physiological processes, we investigate the regulatory role of NAT10 in cell cycle checkpoints, coordination of chromatin remodeling, and detailed modulation of the delicate balance between apoptosis and cell survival. Perturbations in NAT10 expression and function have been linked to oncogenesis, metastasis, and drug resistance in a variety of cancer types. Furthermore, the bewildering interactions between NAT10 and key oncogenic factors, such as p53 and c-Myc, are deciphered, providing profound insights into the molecular underpinnings of cancer pathogenesis. Equally intriguing, the paradoxical role of NAT10 as a potential tumor suppressor or oncogene is influenced by context-dependent factors and the cellular microenvironment. This study explores the fascinating interplay of genetic changes, epigenetic changes, and post-translational modifications that shape the dual character of NAT10, revealing the delicate balance between cancer initiation and suppression. Taken together, this overview delves deeply into the enigmatic role of NAT10 in cancer, elucidating its multifaceted roles and its complex interplay with oncogenic networks.
摘要：
N-乙酰转移酶10(NAT10),一种多才多艺的酶，作为复杂的癌症生物学领域的重要参与者，已经获得了相当多的关注。它在肿瘤发生中的神秘作用跨越了广泛的细胞过程，影响细胞生长，分化,生存,和基因组稳定性。在复杂的致癌信号网络中，NAT10成为多种癌症类型的关键因子，如乳房，肺，结直肠,和白血病。这项引人注目的研究解决了NAT10在癌症发展中的机制作用的复杂复杂性。通过阐明其在基本生理过程中的积极参与，我们研究了NAT10在细胞周期检查点中的调节作用，染色质重塑的协调，以及细胞凋亡和细胞存活之间微妙平衡的详细调节。NAT10表达和功能的扰动与肿瘤发生有关，转移,以及多种癌症类型的耐药性。此外，NAT10和关键致癌因子之间令人困惑的相互作用，如p53和c-Myc，被破译，为癌症发病机制的分子基础提供深刻的见解。同样有趣的是，NAT10作为潜在的肿瘤抑制因子或癌基因的矛盾作用受环境依赖性因素和细胞微环境的影响.这项研究探索了基因变化的迷人相互作用，表观遗传变化,以及塑造NAT10双重特征的翻译后修饰，揭示了癌症起始和抑制之间的微妙平衡。一起来看,本概述深入探讨了NAT10在癌症中的神秘作用，阐明其多方面的作用及其与致癌网络的复杂相互作用。
