综合应力响应
ATF4
mTORC1型
癌症研究
eIF2
生物
细胞周期
细胞生长
P70-S6激酶1
磷酸化
信号转导
未折叠蛋白反应
细胞生物学
细胞凋亡
翻译(生物学)
PI3K/AKT/mTOR通路
内质网
生物化学
基因
信使核糖核酸
作者
Min-Jung Kim,Jinsook Kwak,Hyung Seok Kim,Jihyung Han,Ji An Kang,Jeyun Jo,Jisu Kim,Da Jung Kim,Ho Sup Lee,Hwayoung Yun,Jee‐Yeong Jeong
标识
DOI:10.1158/1535-7163.mct-24-0998
摘要
We investigated the therapeutic potential and mechanisms of HR-19011, a novel eukaryotic translation initiation factor 2 subunit α (eIF2α) phosphorylation inducer, with a focus on its effects on the integrated stress response (ISR) pathway and cell-cycle regulation in K562 cells. Our findings revealed that HR-19011 exerts its anticancer effects primarily through the activation of heme-regulated inhibitor (HRI), leading to the phosphorylation of eIF2α, the induction of ISR signaling, and subsequent G1/S cell-cycle arrest. RNA sequencing analysis further highlighted significant changes in gene expression associated with the ISR pathway, particularly those involving the key components, activating transcription factor 4 and CHOP, underscoring the specific targeting of HRI by HR-19011. Additionally, HR-19011 suppressed the mTORC1 pathway, a critical regulator of cell growth and metabolism, through the downregulation of components such as phosphorylated S6K and phosphorylated 4EBP1, mediated by activating transcription factor 4 and CHOP. In vivo studies demonstrated that HR-19011 effectively inhibited tumor growth in a K562 xenograft model, without significant toxicity, and its broad efficacy across various hematologic malignancies further suggests its potential as a versatile anticancer agent. Our findings position HR-19011 as a promising candidate for targeting the HRI-eIF2α axis in cancer treatment, warranting further investigation and optimization for clinical application.
科研通智能强力驱动
Strongly Powered by AbleSci AI