Laboratorio de Biología Celular del Cáncer, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas s/n Chilpancingo, Gro. 39090, Mexico.
Laboratorio de Biomedicina Molecular, Facultad de Ciencias Químico Biológicas, Universidad Autónoma de Guerrero, Av. Lázaro Cárdenas s/n Chilpancingo, Gro. 39090, Mexico.
Int J Mol Sci. 2019 Jun 13;20(12):2885. doi: 10.3390/ijms20122885.
Epithelial-mesenchymal transition (EMT) is a reversible cellular process, characterized by changes in gene expression and activation of proteins, favoring the trans-differentiation of the epithelial phenotype to a mesenchymal phenotype. This process increases cell migration and invasion of tumor cells, progression of the cell cycle, and resistance to apoptosis and chemotherapy, all of which support tumor progression. One of the signaling pathways involved in tumor progression is the MAPK pathway. Within this family, the ERK subfamily of proteins is known for its contributions to EMT. The ERK subfamily is divided into typical (ERK 1/2/5), and atypical (ERK 3/4/7/8) members. These kinases are overexpressed and hyperactive in various types of cancer. They regulate diverse cellular processes such as proliferation, migration, metastasis, resistance to chemotherapy, and EMT. In this context, in vitro and in vivo assays, as well as studies in human patients, have shown that ERK favors the expression, function, and subcellular relocalization of various proteins that regulate EMT, thus promoting tumor progression. In this review, we discuss the mechanistic roles of the ERK subfamily members in EMT and tumor progression in diverse biological systems.
上皮-间充质转化（EMT）是一种可逆的细胞过程，其特征在于基因表达的变化和蛋白的激活，有利于上皮表型向间充质表型的转分化。这个过程增加了肿瘤细胞的迁移和侵袭、细胞周期的进展以及对细胞凋亡和化疗的抵抗力，所有这些都支持肿瘤的进展。参与肿瘤进展的信号通路之一是 MAPK 通路。在这个家族中，ERK 亚家族的蛋白以其对 EMT 的贡献而闻名。ERK 亚家族分为典型（ERK1/2/5）和非典型（ERK3/4/7/8）成员。这些激酶在各种类型的癌症中过度表达和过度活跃。它们调节多种细胞过程，如增殖、迁移、转移、对化疗的抵抗力和 EMT。在这种情况下，体外和体内实验以及对人类患者的研究表明，ERK 有利于调节 EMT 的各种蛋白的表达、功能和亚细胞重定位，从而促进肿瘤的进展。在这篇综述中，我们讨论了 ERK 亚家族成员在 EMT 和不同生物系统中的肿瘤进展中的机制作用。
