Dual-specificity tyrosine phosphorylation-regulated kinase 1A (DYRK1A) is a dual kinase that can phosphorylate its own activation loop on tyrosine residue and phosphorylate its substrates on threonine and serine residues. It is the most studied member of DYRK kinases, because its gene maps to human chromosome 21 within the Down syndrome critical region (DSCR). DYRK1A overexpression was found to be responsible for the phenotypic features observed in Down syndrome such as mental retardation, early onset neurodegenerative, and developmental heart defects. Besides its dual activity in phosphorylation, DYRK1A carries the characteristic of duality in tumorigenesis. Many studies indicate its possible role as a tumor suppressor gene; however, others prove its pro-oncogenic activity. In this review, we will focus on its multifaceted role in tumorigenesis by explaining its participation in some cancer hallmarks pathways such as proliferative signaling, transcription, stress, DNA damage repair, apoptosis, and angiogenesis, and finally, we will discuss targeting DYRK1A as a potential strategy for management of cancer and neurodegenerative disorders.

双特异性酪氨酸磷酸化调节激酶 1A (DYRK1A) 是一种双激酶，可以磷酸化其自身酪氨酸残基上的激活环，并磷酸化其苏氨酸和丝氨酸残基上的底物。它是 DYRK 激酶中研究最多的成员，因为其基因映射到唐氏综合症关键区域 (DSCR) 内的人类 21 号染色体。 DYRK1A过度表达被发现与唐氏综合症中观察到的表型特征有关，例如智力低下、早发性神经退行性疾病和发育性心脏缺陷。除了磷酸化的双重活性外，DYRK1A 还具有肿瘤发生的双重特征。许多研究表明它可能作为肿瘤抑制基因发挥作用；然而，其他人证明了它的促癌活性。在这篇综述中，我们将通过解释其参与一些癌症标志通路（如增殖信号传导、转录、应激、DNA 损伤修复、细胞凋亡和血管生成）来重点关注其在肿瘤发生中的多方面作用，最后，我们将讨论将 DYRK1A 作为靶向药物治疗癌症和神经退行性疾病的潜在策略。