CDH1
脱甲基酶
癌基因
基因敲除
基因沉默
上皮-间质转换
癌症研究
钙粘蛋白
癌症
下调和上调
赖氨酸
细胞生长
分子医学
化学
细胞
细胞培养
生物
细胞周期
医学
基因
内科学
遗传学
氨基酸
生物化学
表观遗传学
作者
Deguan Li,Shangxin Zhang,Qiang Yan,Yongxiang Li
标识
DOI:10.2174/1389201024666230320100504
摘要
Gastric cancer (GC) ranks fifth among all common malignancies globally. Genetic research has revealed several genes that are frequently dis-regulated in GC, such as lysine-specific demethylase 6A (KDM6A) and cadherin-1 (CDH1).This study aimed to examine the expression profile and role of KDM6A in GC, as well as the molecular pathway involved.The expression profile and overall survival data of KDM6A were retrieved from the TCGA database. Expression levels of KDM6A were also measured in GC patient samples and compared with those of healthy controls. Furthermore, stable silencing of KDM6A was introduced into the GC cell line NCI-N87, followed by assessments of cell proliferation, migration and invasion, in the xenograft mouse model. The metastatic status of mice injected with NCI-N87 cells was also analyzed.In patients diagnosed with GC, KDM6A was upregulated. Silencing KDM6A reduced the proliferation, migration and invasion of cells, as well as the growth of xenograft tumors. KDM6A knockdown also inhibited metastatic behaviors of injected NCI-N87 cells, as well as elevated CDH1 expression, leading to reversed epithelial-mesenchymal transition.KDM6A serves as an oncogene in GC and exerts its pro-tumor functions by repressing the expression of CDH1.
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