Epidermal growth factor receptor (EGFR) is a transmembrane glycoprotein that possesses intrinsic tyrosine kinase activity. EGFR signaling dysregulation is vital to tumor progression.¹ EGFR is considered a cancer-driving gene that affects numerous systems involved in oncogenesis, including cell proliferation, DNA synthesis, cell cycle progression, invasion, and metastasis.² Hyperactivation of the EGFR pathway in NSCLC has been shown to result in the development of many cancer characteristics, such as increased cell proliferation, migration, angiogenesis, metastasis, and increased cell survival by blocking apoptosis.^3–5 Many chemical inhibitors of EGFR and EGFR-neutralizing antibodies have been developed for cancer therapy.^6,7 However, their effects in the treatment of NSCLC are not very satisfactory likely because the mechanisms driving NSCLC progression are not fully understood.⁸ Thus, the detailed molecular mechanisms of the role of EGFR-related pathways in NSCLC progression remain to be elucidated.

中文翻译：

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p53/miR-193a/EGFR反馈环路作为非小细胞肺癌肿瘤发生的驱动力


表皮生长因子受体（EGFR）是一种跨膜糖蛋白，具有内在的酪氨酸激酶活性。 EGFR 信号传导失调对于肿瘤进展至关重要。 ¹ EGFR 被认为是一种癌症驱动基因，影响涉及肿瘤发生的众多系统，包括细胞增殖、DNA 合成、细胞周期进展、侵袭和转移。 ² NSCLC 中 EGFR 通路的过度激活已被证明会导致许多癌症特征的发展，例如细胞增殖、迁移、血管生成、转移增加以及通过阻止细胞凋亡增加细胞存活率。 ^3-5许多 EGFR 化学抑制剂和 EGFR 中和抗体已被开发用于癌症治疗。 ^6,7然而，它们在 NSCLC 治疗中的效果并不十分令人满意，可能是因为驱动 NSCLC 进展的机制尚未完全了解。 ⁸因此，EGFR 相关通路在 NSCLC 进展中的作用的详细分子机制仍有待阐明。