Seres Mario, Spacayova Katarina, Sulova Zdena, Spaldova Jana, Breier Albert, Pavlikova Lucia
Institute of Molecular Physiology and Genetics, Centre of Bioscience, Slovak Academy of Sciences, Dúbravská Cesta 9, 84005 Bratislava, Slovakia.
Department of Molecular Biology, Faculty of Natural Sciences, Comenius University, Ilkovičova 6, 84215 Bratislava, Slovakia.
Cancers (Basel). 2025 Jan 14;17(2):248. doi: 10.3390/cancers17020248.
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. The and oncogenes 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节基因表达：作为细胞核中的生长因子，在与配体结合后易位至此；或通过其在细胞质中的内在酪氨酸激酶活性，在此调节关键信号通路，如RAS/MYC、PI3K、PLCγ和STAT3。在肿瘤发生过程中，这些通路失调，导致不受控制的增殖、增强的迁移和转移能力、逃避程序性细胞死亡以及对化疗或放疗产生抗性。 癌基因和 癌基因在肿瘤发生中起关键作用，驱动诸如抗凋亡、复制永生、细胞侵袭和转移以及代谢重编程等过程。这些癌基因受到一系列表观遗传和转录后修饰的调控。本综述重点关注由（表观）遗传改变和翻译后修饰导致的EGFR、RAS和MYC表达失调。它还探讨了靶向这些调节蛋白的治疗潜力，强调对肿瘤组织进行表型分析以指导癌症治疗的重要性。
