癌症研究
信号转导
下调和上调
磷酸化
激酶
酪氨酸激酶
癌基因
细胞生长
生物
受体酪氨酸激酶
肝细胞癌
酪氨酸激酶抑制剂
化学
癌细胞
酪氨酸
蛋白激酶A
细胞周期
蛋白酪氨酸激酶
癌症
细胞培养
细胞
基因
基因表达调控
肝细胞
细胞生物学
转染
HEK 293细胞
基因表达
分子生物学
作者
Yali Xu,Hricha Mishra,Hiroyuki Osada,Nobumoto Watanabe,Hiroyuki Hirano,Hajime Nishimura,Yutaka Furutani,Yusuke Suenaga,Yoshitaka Hippo,Wenkui Yu,Harukazu Suzuki,Xian‐Yang Qin
标识
DOI:10.1021/acschembio.5c00675
摘要
suppression. Notably, MI102 effect exhibited superior tumor cell selectivity compared with the MET inhibitor tivantinib. At the transcriptional level, RNA-seq revealed that MI102 globally downregulated MYCN-associated oncogenic programs. Collectively, these findings establish pharmacological downregulation of MYCN as a promising therapeutic strategy for HCC and reveal a functional link between MET signaling and MYCN-driven oncogenic pathways.
科研通智能强力驱动
Strongly Powered by AbleSci AI