Department of Pathophysiology, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, 450000, China.
Tianjian Laboratory for Advanced Biomedical Sciences, Zhengzhou, 450052, Henan, China.
Mol Cancer. 2023 Dec 18;22(1):208. doi: 10.1186/s12943-023-01903-x.
The RAS/mitogen-activated protein kinase (MAPK) signaling cascade is commonly dysregulated in human malignancies by processes driven by RAS or RAF oncogenes. Among the members of the RAF kinase family, CRAF plays an important role in the RAS-MAPK signaling pathway, as well as in the progression of cancer. Recent research has provided evidence implicating the role of CRAF in the physiological regulation and the resistance to BRAF inhibitors through MAPK-dependent and MAPK-independent mechanisms. Nevertheless, the effectiveness of solely targeting CRAF kinase activity remains controversial. Moreover, the kinase-independent function of CRAF may be essential for lung cancers with KRAS mutations. It is imperative to develop strategies to enhance efficacy and minimize toxicity in tumors driven by RAS or RAF oncogenes. The review investigates CRAF alterations observed in cancers and unravels the distinct roles of CRAF in cancers propelled by diverse oncogenes. This review also seeks to summarize CRAF-interacting proteins and delineate CRAF's regulation across various cancer hallmarks. Additionally, we discuss recent advances in pan-RAF inhibitors and their combination with other therapeutic approaches to improve treatment outcomes and minimize adverse effects in patients with RAF/RAS-mutant tumors. By providing a comprehensive understanding of the multifaceted role of CRAF in cancers and highlighting the latest developments in RAF inhibitor therapies, we endeavor to identify synergistic targets and elucidate resistance pathways, setting the stage for more robust and safer combination strategies for cancer treatment.
RAS/丝裂原活化蛋白激酶(MAPK)信号级联在人类恶性肿瘤中通常通过 RAS 或 RAF 癌基因驱动的过程失调。在 RAF 激酶家族的成员中, CRAF 在 RAS-MAPK 信号通路以及癌症进展中发挥重要作用。最近的研究提供了证据,表明 CRAF 通过 MAPK 依赖性和非 MAPK 依赖性机制在生理调节和 BRAF 抑制剂耐药性中发挥作用。然而,仅靶向 CRAF 激酶活性的有效性仍然存在争议。此外,CRAF 的激酶非依赖性功能对于具有 KRAS 突变的肺癌可能是必不可少的。开发策略以增强 RAS 或 RAF 癌基因驱动的肿瘤的疗效并最小化毒性至关重要。本综述调查了癌症中观察到的 CRAF 改变,并揭示了 CRAF 在不同癌基因驱动的癌症中的独特作用。本综述还旨在总结 CRAF 相互作用蛋白,并描述 CRAF 在各种癌症特征中的调节。此外,我们讨论了泛 RAF 抑制剂的最新进展及其与其他治疗方法的联合应用,以改善 RAF/RAS 突变肿瘤患者的治疗效果并最小化不良反应。通过全面了解 CRAF 在癌症中的多方面作用,并强调 RAF 抑制剂治疗的最新进展,我们努力确定协同作用靶点并阐明耐药途径,为癌症治疗制定更强大和更安全的联合策略奠定基础。