The epidermal growth factor receptor (EGFR) regulates gene expression through two primary mechanisms: as a growth factor in the nucleus, where it translocates upon binding its ligand, or via its intrinsic tyrosine kinase activity in the cytosol, where it modulates key signaling pathways such as RAS/MYC, PI3K, PLCγ, and STAT3. During tumorigenesis, these pathways become deregulated, leading to uncontrolled proliferation, enhanced migratory and metastatic capabilities, evasion of programmed cell death, and resistance to chemotherapy or radiotherapy. TheRASandMYConcogenes are pivotal in tumorigenesis, driving processes such as resistance to apoptosis, replicative immortality, cellular invasion and metastasis, and metabolic reprogramming. These oncogenes are subject to regulation by a range of epigenetic and post-transcriptional modifications. This review focuses on the deregulation of EGFR, RAS, and MYC expression caused by (epi)genetic alterations and post-translational modifications. It also explores the therapeutic potential of targeting these regulatory proteins, emphasizing the importance of phenotyping neoplastic tissues to inform the treatment of cancer.
表皮生长因子受体（EGFR）通过两种主要机制调控基因表达：一是作为生长因子在细胞核内发挥作用，其在配体结合后发生核转位；二是通过其胞质内的固有酪氨酸激酶活性，调控RAS/MYC、PI3K、PLCγ及STAT3等关键信号通路。在肿瘤发生过程中，这些通路发生失调，导致细胞增殖失控、迁移与转移能力增强、程序性细胞死亡逃逸以及对化疗或放疗的抵抗。RAS与MYC原癌基因在肿瘤发生中具有核心作用，驱动细胞凋亡抵抗、复制永生、侵袭转移及代谢重编程等过程。这些癌基因受到多种表观遗传及转录后修饰的调控。本综述重点探讨由（表观）遗传改变与翻译后修饰引起的EGFR、RAS及MYC表达失调，并深入分析靶向这些调控蛋白的治疗潜力，强调对肿瘤组织进行表型分析对指导癌症治疗的重要意义。
肿瘤(癌症)患者之家