信号通路调控上皮间质转化抑制乳腺癌转移的研究探索

Research Exploration on the Regulation of Epithelial-Mesenchymal Transition by Signaling Pathways to Inhibit Breast Cancer Metastasis

摘要: 乳腺癌，这一学术领域内被广泛研究的恶性肿瘤，作为严重威胁女性健康的疾病，其进展与上皮间质转化(EMT)密切相关。EMT通过多层次调控网络驱动肿瘤侵袭转移，其中TGFβ/Smad通路呈现早期抑制、晚期激活EMT的时序性调控特征，与Wnt/β-catenin通路形成动态互作。AKT/GSK3β/Snail轴通过磷酸化级联调控转录因子，CXCL3/CXCR2轴经自/旁分泌激活下游信号，协同构建多维EMT调控体系。本研究系统解析上述核心通路的分子互作网络，阐明关键效应因子的生化机制及时空动态规律，旨在为乳腺癌早期分子标志物筛选及靶向治疗提供理论支撑，推动基于EMT节点干预的新型诊疗策略开发。

Abstract: Breast cancer, a malignant tumor widely studied in the academic field, as a disease seriously threatening women’s health, its progression is closely related to epithelial-mesenchymal transition (EMT). EMT drives tumor invasion and metastasis through a multi-level regulatory network. Among them, the TGFβ/Smad pathway shows the sequential regulatory characteristics of early inhibition and late activation of EMT, and forms a dynamic interaction with the Wnt/β-catenin pathway. The AKT/GSK3β/Snail axis regulates transcription factors through a phosphorylation cascade, while the CXCL3/CXCR2 axis activates downstream signals through autocrine/paracrine secretion, jointly constructing a multi-dimensional EMT regulatory system. This study systematically analyzed the molecular interaction networks of the above-mentioned core pathways, clarified the biochemical mechanisms and spatiotemporal dynamic laws of key effect factors, aiming to provide theoretical support for the screening of early molecular markers and targeted therapy of breast cancer, and promote the development of new diagnosis and treatment strategies based on EMT node intervention.