蛋白酪氨酸激酶 (PTK) 除了作为治疗包括癌症在内的许多人类疾病的治疗靶点外，还充当信号传导通路中的关键分子。 PTK 的特点是能够磷酸化丝氨酸、苏氨酸或酪氨酸残基，从而可以快速、可逆地改变其蛋白质底物的功能，其形式是蛋白质确认和与蛋白质伴侣相互作用的亲和力发生显着变化，从而驱动细胞功能。正常和病理条件。 PTK 分为两组：一组代表酪氨酸激酶，另一组包括丝氨酸/苏氨酸激酶的成员。酪氨酸激酶组被细分为亚组：其中一个亚组包括受体酪氨酸激酶（RTK）成员，而另一个亚组包括非受体酪氨酸激酶（NRTK）成员。这两个激酶组在许多细胞功能中充当“开”或“关”开关。 NRTK 是在许多癌症类型中过度表达和激活的酶，并根据细胞外信号传导依赖性机制调节可变的细胞功能。 NRTK 介导的不同细胞功能由细胞质或细胞核中的激酶依赖性和激酶非依赖性机制调节。因此，靶向NRTK对于改善不同肿瘤类型的治疗策略具有重要意义。本综述讨论了 NRTK 在肿瘤进展和耐药中的结构和机制作用，以及它们作为肿瘤治疗靶点的重要性。

Protein tyrosine kinases (PTKs) function as key molecules in the signaling pathways in addition to their impact as a therapeutic target for the treatment of many human diseases, including cancer. PTKs are characterized by their ability to phosphorylate serine, threonine, or tyrosine residues and can thereby rapidly and reversibly alter the function of their protein substrates in the form of significant changes in protein confirmation and affinity for their interaction with protein partners to drive cellular functions under normal and pathological conditions. PTKs are classified into two groups: one of which represents tyrosine kinases, while the other one includes the members of the serine/threonine kinases. The group of tyrosine kinases is subdivided into subgroups: one of them includes the member of receptor tyrosine kinases (RTKs), while the other subgroup includes the member of non-receptor tyrosine kinases (NRTKs). Both these kinase groups function as an "on" or "off" switch in many cellular functions. NRTKs are enzymes which are overexpressed and activated in many cancer types and regulate variable cellular functions in response to extracellular signaling-dependent mechanisms. NRTK-mediated different cellular functions are regulated by kinase-dependent and kinase-independent mechanisms either in the cytoplasm or in the nucleus. Thus, targeting NRTKs is of great interest to improve the treatment strategy of different tumor types. This review deals with the structure and mechanistic role of NRTKs in tumor progression and resistance and their importance as therapeutic targets in tumor therapy.