Cancer is the second leading cause of death worldwide and accounted for an estimated 9.6 million deaths, or 1 in 6 deaths, in 2018. Despite recent advances in cancer prevention, diagnosis, and treatment strategies, the burden of this disease continues to grow with each year, with dire physical, emotional, and economic consequences for all levels of society. Classic characteristics of cancer include rapid, uncontrolled cell proliferation and spread of cancerous cells to other parts of the body, a process known as metastasis. Transient receptor potential melastatin 7 (TRPM7), a Ca²⁺- and Mg²⁺-permeable nonselective divalent cation channel defined by the atypical presence of an α-kinase within its C-terminal domain, has been implicated, due to its modulation of Ca²⁺ and Mg²⁺ influx, in a wide variety of physiological and pathological processes, including cancer. TRPM7 is overexpressed in several cancer types and has been shown to variably increase cellular proliferation, migration, and invasion of tumour cells. However, the relative contribution of TRPM7 kinase domain activity to cancer as opposed to ion flux through its channel pore remains an area of active discovery. In this review, we describe the specific role of the TRPM7 kinase domain in cancer processes as well as mechanisms of regulation and inhibition of the kinase domain.

癌症是全球第二大死因，2018 年估计有 960 万人死亡，占死亡人数的六分之一。年，对社会各阶层造成可怕的身体、情感和经济后果。癌症的典型特征包括快速、不受控制的细胞增殖和癌细胞向身体其他部位的扩散，这一过程被称为转移。瞬时受体电位 melastatin 7 (TRPM7) 是一种 Ca ²⁺ - 和 Mg ²⁺可渗透的非选择性二价阳离子通道，由其 C 端结构域内 α-激酶的非典型存在定义，由于其调节钙²⁺和 Mg ²⁺流入，在各种生理和病理过程中，包括癌症。TRPM7 在几种癌症类型中过度表达，并已显示出不同程度地增加肿瘤细胞的细胞增殖、迁移和侵袭。然而，与通过其通道孔的离子通量相反，TRPM7 激酶结构域活性对癌症的相对贡献仍然是一个积极发现的领域。在这篇综述中，我们描述了 TRPM7 激酶结构域在癌症过程中的具体作用以及激酶结构域的调节和抑制机制。