经典的丝裂原激活蛋白激酶 (MAPK) 信号通路 Ras/Raf/MEK（丝裂原激活蛋白激酶/ERK 激酶）/ERK 蛋白激酶级联是调节细胞生长、分化和增殖的保守级联。 2002年，随着在几种人类肿瘤中发现BRAF的癌症激活突变，BRAF在癌症中的重要性被确立。目前，BRAF被认为是一种驱动突变，以不同的方式影响癌症表型，使其成为癌症的重要治疗靶点。 BRAF 选择性抑制剂在涉及转移性黑色素瘤患者的临床试验中显示出前景。然而，BRAF 抑制剂治疗的耐药机制导致治疗反应短暂。迫切需要进一步深入研究来探索阻碍 BRAF 抑制剂有效性的耐药机制。代谢重编程在 BRAF 突变癌症中发挥着新的作用。特别是，线粒体代谢及其由线粒体介导的密切相关的信号通路已被认为是治疗 BRAF 突变癌症的潜在新靶点。这篇综述探讨了了解癌症中 BRAF 突变的进展、BRAF 抑制剂的临床病理学相关性，以及 BRAF 突变癌症中线粒体代谢、线粒体动力学和线粒体介导的死亡的最新进展。该综述将为未来的癌症研究提供信息，并为 BRAF 突变癌症的新型治疗组合奠定基础。版权所有 © 2024 Elsevier B.V. 保留所有权利。

The classical mitogen-activated protein kinase (MAPK) signaling pathway, the Ras/Raf/MEK (mitogen-activated protein kinase/ERK kinase)/ERK protein kinase cascade, is a conserved cascade that regulates cell growth, differentiation, and proliferation. The significance of BRAF in cancer was established with the discovery of cancer-activating mutations in BRAF in several human tumors in 2002. Currently, BRAF is recognized as a driver mutation that affects cancer phenotypes in different ways, making it an important therapeutic target for cancer. BRAF-selective inhibitors have shown promise in clinical trials involving patients with metastatic melanoma. However, resistance mechanisms to BRAF inhibitors therapy have resulted in short-lived therapeutic responses. Further in-depth research is imperative to explore resistance mechanisms that oppose the effectiveness of BRAF inhibitors. Metabolic reprogramming has emerging role in BRAF-mutant cancers. In particular, mitochondrial metabolism and its closely related signaling pathways mediated by mitochondria have become recognized as potential new targets for treating BRAF-mutant cancers. This review, examines the progress in understanding BRAF mutations in cancer, the clinicopathological correlation of BRAF inhibitors, and recent advances in mitochondrial metabolism, mitochondrial dynamics and mitochondrial mediated death in BRAF-mutant cancer. This review will inform future cancer research and lay the foundation for novel treatment combinations of BRAF-mutant cancers.Copyright © 2024 Elsevier B.V. All rights reserved.