Analysis of the β catenin gene abnormality and therapeutic application for oral cancer.

实体肿瘤中的缺氧区介导恶性转化、癌细胞增殖、对抗癌药物的抵抗以及细胞侵袭和转移的增强。在本研究中，我们发现wnt/β-catenin通路激活介导口腔鳞状细胞癌细胞的侵袭和转移潜能的获得。缺氧可增强葡萄糖转运蛋白1 （GLUT1）的表达和抗肿瘤耐药，激活NF-κB/p65，触发细胞增殖。

Hypoxic regions in solid tumors mediate malignant transformation, cancer cell proliferation, resistance to anti-cancer agents, and enhanced cellular invasion and metastasis. In this study, we found that the wnt/β-catenin pathway activation mediates the acquisition of invasion and metastatic potential in oral squamous cell carcinoma cells. Hypoxia enhances the expression of glucose transporter 1 (GLUT1) and anticancer drug resistance, and activates NF-κB/p65 to trigger cell proliferation.