International Journal of Clinical Research
International Journal of Clinical Research. 2025; 9: (5) ; 10.12208/j.ijcr.20250248 .
总浏览量: 115
承德医学院附属医院外三科 河北承德
*通讯作者: 赵恩宏,单位:承德医学院附属医院外三科 河北承德;
皮质肌动蛋白(Cortactin)通过结合Arp2/3复合体及丝状肌动蛋白(F-actin)调控细胞骨架动态,参与细胞迁移、侵袭和伪足形成。其在结肠直肠癌、膀胱癌和胰腺癌等中过表达的cortactin通过多种机制促进肿瘤发生发展:1)磷酸化修饰调节肌动蛋白重组;2)与Arp2/3复合体协同形成侵袭伪足;3)干扰钙黏蛋白介导的细胞黏附;4)诱导基质金属蛋白酶(MMPs)分泌以降解细胞外基质。Cortactin的表达与肿瘤恶性程度及不良预后密切相关,提示其作为潜在治疗靶点的价值。然而,其在肿瘤发生中的具体因果机制仍需进一步阐明。
Cortactin drives cancer progression by modulating cytoskeletal dynamics. It activates Arp2/3 to nucleate branched actin networks, facilitating invasive protrusions and cell migration. Overexpressed in colorectal, bladder, and pancreatic cancers, cortactin promotes development via multiple mechanisms: 1) phosphorylation-dependent actin remodeling; 2) disruption of E-cadherin-mediated cell-cell adhesion; 3) activation of FAK-Rac1 and MAPK pathways to enhance proliferation; and 4) upregulating MMPs to degrade extracellular matrix. Its overexpression correlates with aggressive tumor behavior and poor patient outcomes, underscoring its therapeutic potential. However, whether cortactin directly initiates tumorigenesis or amplifies existing oncogenic signals remains unclear, necessitating deeper mechanistic studies to establish causality and refine targeting strategies.
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