Lacorazza H Daniel
Department of Pathology and Immunology, Baylor College of Medicine, Houston, TX, United States.
Front Oncol. 2024 Dec 9;14:1486756. doi: 10.3389/fonc.2024.1486756. eCollection 2024.
The MAP2K7 signaling pathway activates the c-Jun NH2-terminal protein kinase (JNK) in response to stress signals, such as inflammatory cytokines, osmotic stress, or genomic damage. While there has been interest in inhibiting JNK due to its involvement in inflammatory processes and cancer, there is increasing focus on developing MAP2K7 inhibitors to enhance specificity when MAP2K7 activation is associated with disease progression. Despite some progress, further research is needed to fully comprehend the role of MAP2K7 in cancer and assess the potential use of kinase inhibitors in cancer therapy. This review examines the role of MAP2K7 in cancer and the development of small-molecule inhibitors.
丝裂原活化蛋白激酶激酶7(MAP2K7)信号通路在响应应激信号(如炎性细胞因子、渗透压应激或基因组损伤)时激活c-Jun氨基末端蛋白激酶(JNK)。尽管由于JNK参与炎症过程和癌症而对其抑制产生了兴趣,但当MAP2K7激活与疾病进展相关时,人们越来越关注开发MAP2K7抑制剂以提高特异性。尽管取得了一些进展,但仍需要进一步研究以全面理解MAP2K7在癌症中的作用,并评估激酶抑制剂在癌症治疗中的潜在用途。本综述探讨了MAP2K7在癌症中的作用以及小分子抑制剂的开发。