大量的生化反应导致细胞增殖改变，进而引起肿瘤发生和抗癌治疗抵抗。涉及的机制包括基因和表观遗传变化、细胞内信号传导的改变以及内在和外在因素导致的控制机制失效。没有唯一的生化事件负责；缠绕在一起的分子反应使组织中的细胞表现出无控制的生长和异常迁移。大量的实验研究支持了NK-1R（神经激肽-1受体）的活化在不同组织中致癌现象的病因责任，无论是独立地还是与其他机制合作。因此，在恶性进程的背景下，深入研究该受体系统对于设计针对NK-1R偏离活性的新治疗手段至关重要。本研究回顾和讨论了最近的文献，分析了神经激肽1全长和截短受体变体活化所影响的主要信号通路。此外，还讨论了NK-1R在癌症发展中的参与情况。NK-1R能通过多种途径进行信号传导并与其他受体系统交互。在不同类型的癌症中，超越或功能失常的NK-1R在恶性进程中的参与需要更精确的定义，以应用令人满意、有效的治疗方法。我们已经走了很长的路：目前已经有选择性和有效的NK-1R拮抗剂，并且有能力基于受体的结构状态和功能意义开发具有偏向激动性属性的新药物，这使得立即的科研行动和临床应用成为可能。版权所有© Bentham Science Publishers；如有任何问题，请发送电子邮件至epub@benthamscience.net。

Numerous biochemical reactions leading to altered cell proliferation cause tumorigenesis and cancer treatment resistance. The mechanisms implicated include genetic and epigenetic changes, modified intracellular signaling, and failure of control mechanisms caused by intrinsic and extrinsic factors alone or combined. No unique biochemical events are responsible; entangled molecular reactions conduct the resident cells in a tissue to display uncontrolled growth and abnormal migration. Copious experimental research supports the etiological responsibility of NK-1R (neurokinin-1 receptor) activation, alone or cooperating with other mechanisms, in cancer appearance in different tissues. Consequently, a profound study of this receptor system in the context of malignant processes is essential to design new treatments targeting NK-1R-deviated activity.This study reviews and discusses recent literature that analyzes the main signaling pathways influenced by the activation of neurokinin 1 full and truncated receptor variants. Also, the involvement of NK-1R in cancer development is discussed.NK-1R can signal through numerous pathways and cross-talk with other receptor systems. The participation of override or malfunctioning NK-1R in malignant processes needs a more precise definition in different types of cancers to apply satisfactory and effective treatments. A long way has already been traveled: the current disposal of selective and effective NK-1R antagonists and the capacity to develop new drugs with biased agonistic properties based on the receptor's structural states with functional significance opens immediate research action and clinical application.Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.