脂肪酸结合蛋白7(FABP7)是参与摄取的细胞内蛋白,交通运输,新陈代谢,和脂肪酸(FAs)的储存。FABP7在多种癌症中上调高达20倍,通常与不良预后相关。FABP7沉默或药理抑制表明FABP7促进细胞生长,迁移,入侵,菌落和球体形成/增加的大小,脂质摄取,和脂滴形成。异种移植研究表明,抑制FABP7抑制肿瘤形成和肿瘤生长,并提高宿主的存活率。分子机制涉及促进FA摄取,脂滴,信号[粘着斑激酶(FAK),原癌基因酪氨酸蛋白激酶Src(Src),丝裂原活化蛋白激酶激酶/p-细胞外信号调节激酶(MEK/ERK),和Wnt/β-catenin],缺氧诱导因子1-α(Hif1α),血管内皮生长因子A/脯氨酸4-羟化酶亚基α-1(VEGFA/P4HA1),蜗牛家族锌指1(Snail1),和扭曲相关蛋白1(Twist1)。FABP7的致癌能力使其成为未来癌症治疗的有希望的药理学靶标。
Fatty acid binding protein 7 (FABP7) is an intracellular protein involved in the uptake, transportation, metabolism, and storage of fatty acids (FAs). FABP7 is upregulated up to 20-fold in multiple cancers, usually correlated with poor prognosis. FABP7 silencing or pharmacological inhibition suggest FABP7 promotes cell growth, migration, invasion, colony and spheroid formation/increased size, lipid uptake, and lipid droplet formation. Xenograft studies show that suppression of FABP7 inhibits tumour formation and tumour growth, and improves host survival. The molecular mechanisms involve promotion of FA uptake, lipid droplets, signalling [focal adhesion kinase (FAK), proto-oncogene tyrosine-protein kinase Src (Src), mitogen-activated protein kinase kinase/p-extracellular signal-regulated kinase (MEK/ERK), and Wnt/β-catenin], hypoxia-inducible factor 1-alpha (Hif1α), vascular endothelial growth factor A/prolyl 4-hydroxylase subunit alpha-1 (VEGFA/P4HA1), snail family zinc finger 1 (Snail1), and twist-related protein 1 (Twist1). The oncogenic capacity of FABP7 makes it a promising pharmacological target for future cancer treatments.