本研究旨在阐明LINC00663/EBF1/NR2F1轴对膀胱癌(BC)炎症和血管生成的影响及其相关分子机制。转染后,进行功能实验以测试细胞增殖和侵袭,成管能力,和炎症因子的含量,蜗牛,E-cadherin,和VEGFA。同时,预测并验证了LINC00663、EBF1和NR2F1之间的关系。此外,在裸鼠中进行异种移植实验以观察体内5637BC细胞的致癌性。在BC组织和细胞中,LINC00663和NR2F1上调。沉默NR2F1或LINC00663抑制细胞增殖和侵袭,体外减弱的血管拟态,炎症因子降低,蜗牛,和VEGFA水平,E-cadherin的表达增加。LINC00663通过EBF1正调控NR2F1的表达。此外,体内实验表明,NR2F1上调逆转了LINC00663沉默对肿瘤生长的抑制作用,炎症,和血管生成。沉默LINC00663通过介导EBF1降低NR2F1表达,从而抑制BC炎症和血管生成。
This study is to elucidate the effect of the LINC00663/
EBF1/NR2F1 axis on inflammation and angiogenesis in bladder cancer (BC) and related molecular mechanisms. After transfection, functional experiments were conducted to test cell proliferation and invasion, tube formation ability, and content of inflammatory factors, Snail, E-cadherin, and VEGFA. Meanwhile, the relationships among LINC00663,
EBF1, and NR2F1 were predicted and verified. In addition, xenograft experiments in nude mice were performed to observe the oncogenicity of 5637 BC cells in vivo. In BC tissues and cells, LINC00663 and NR2F1 were upregulated. Silencing NR2F1 or LINC00663 repressed cell proliferation and invasion, weakened vascular mimicry in vitro, decreased inflammatory factor, Snail, and VEGFA levels, and increased expression of E-cadherin. LINC00663 positively regulated NR2F1 expression through
EBF1. Additionally, in vivo experiments showed that NR2F1 upregulation reversed the suppression effects of LINC00663 silencing on tumour growth, inflammation, and angiogenesis. Silencing LINC00663 decreased NR2F1 expression by mediating
EBF1, thereby inhibiting BC inflammation and angiogenesis.