Inhibition of PTPRE suppresses tumor progression and improves sorafenib response in hepatocellular carcinoma

被引:3
|
作者
Dong, Renshun [1 ,2 ,3 ]
Wang, Tianci [1 ,2 ,3 ]
Dong, Wei [1 ,2 ,3 ,4 ,5 ,6 ]
Zhu, He [1 ,2 ,3 ,4 ,5 ,6 ]
Liu, Qiumeng [1 ,2 ,3 ,4 ,5 ]
Liang, Huifang [1 ,2 ,3 ,4 ,5 ,6 ]
Chen, Xiaoping [1 ,2 ,3 ,4 ,5 ,6 ]
Zhang, Bixiang [1 ,2 ,3 ,4 ,5 ,6 ]
Zhang, Xuewu [1 ,2 ,3 ,4 ,5 ,6 ]
机构
[1] Huazhong Univ Sci & Technol, Tongji Hosp, Tongji Med Coll, Hepat Surg Ctr, Wuhan 430030, Hubei, Peoples R China
[2] Hubei Key Lab Hepatopancreato Biliary Dis, Wuhan 430030, Hubei, Peoples R China
[3] Hubei Prov Clin Med Res Ctr Hepat Surg, Wuhan 430030, Hubei, Peoples R China
[4] Minist Educ, Key Lab Organ Transplantat, Wuhan 430030, Hubei, Peoples R China
[5] Chinese Acad Med Sci, NHC Key Lab Organ Transplantat, Wuhan 430030, Hubei, Peoples R China
[6] Chinese Acad Med Sci, Key Lab Organ Transplantat, Wuhan 430030, Hubei, Peoples R China
基金
中国国家自然科学基金;
关键词
PTPRE inhibitor; Hepatocellular carcinoma; Sorafenib; Organoid; OPEN-LABEL; PLUS; ATEZOLIZUMAB; BEVACIZUMAB; METABOLISM; MYC;
D O I
10.1016/j.biopha.2024.116366
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Hepatocellular carcinoma (HCC) has a poor prognosis, and the efficacy of current therapeutic strategies is extremely limited in advanced diseases. Our previous study reported that protein tyrosine phosphatase receptor epsilon (PTPRE) is a promoting factor in HCC progression. In this study, our objective was to evaluate the treatment effect of PTPRE inhibitors in different HCC preclinical models. Our results indicated that the PTPRE inhibitory compound 63 (Cpd-63) inhibited tumor cell proliferation, migration, and HCC organoid growth. Mechanism research revealed that Cpd-63 could inhibit the expression of MYC and MYC targets by inhibiting the activation of SRC. Additionally, we found that Cpd-63 could improve the response of sorafenib in HCC cells. In conclusion, we demonstrated that the PTPRE inhibitors represented a potential therapeutic agent for HCC management.
引用
收藏
页数:11
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