scholarly journals 6‐Methoxyethylamino‐numonafide inhibits hepatocellular carcinoma xenograft growth as a single agent and in combination with sorafenib

2017 ◽  
Vol 31 (12) ◽  
pp. 5453-5465 ◽  
Author(s):  
Yanning Liu ◽  
Guohua Lou ◽  
John T. Norton ◽  
Chen Wang ◽  
Irawati Kandela ◽  
...  
Hepatology ◽  
2011 ◽  
Vol 54 (6) ◽  
pp. 2036-2047 ◽  
Author(s):  
Xin Zeng ◽  
Yong Lin ◽  
Chuan Yin ◽  
Xin Zhang ◽  
Bei-Fang Ning ◽  
...  

2012 ◽  
Vol 44 (1) ◽  
pp. 98-101 ◽  
Author(s):  
Premal D. Lulla ◽  
Jonathan E. Brammer ◽  
Salman Bandeali ◽  
Garret R. Lynch

2008 ◽  
Vol 16 (33) ◽  
pp. 3713
Author(s):  
Jian-Yong Zhang ◽  
Jin-Yi Li ◽  
Hong-Yu Li ◽  
Cong Dai ◽  
Chun-Lei Ma ◽  
...  

Oncotarget ◽  
2015 ◽  
Vol 6 (24) ◽  
pp. 20160-20176 ◽  
Author(s):  
Qingyang Gu ◽  
Bin Zhang ◽  
Hongye Sun ◽  
Qiang Xu ◽  
Yexiong Tan ◽  
...  

Cancer ◽  
2012 ◽  
Vol 118 (21) ◽  
pp. 5293-5301 ◽  
Author(s):  
Joanne Chiu ◽  
Yuen Fong Tang ◽  
Tzy-Jyun Yao ◽  
Ashley Wong ◽  
Hilda Wong ◽  
...  

2021 ◽  
Vol 13 (579) ◽  
pp. eabb6282
Author(s):  
Fan-En Kong ◽  
Guang-Meng Li ◽  
Yun-Qiang Tang ◽  
Shao-Yan Xi ◽  
Jane Ho Chun Loong ◽  
...  

Tumor lineage plasticity is emerging as a critical mechanism of therapeutic resistance and tumor relapse. Highly plastic tumor cells can undergo phenotypic switching to a drug-tolerant state to avoid drug toxicity. Here, we investigate the transmembrane tight junction protein Claudin6 (CLDN6) as a therapeutic target related to lineage plasticity for hepatocellular carcinoma (HCC). CLDN6 was highly expressed in embryonic stem cells but markedly decreased in normal tissues. Reactivation of CLDN6 was frequently observed in HCC tumor tissues as well as in premalignant lesions. Functional assays indicated that CLDN6 is not only a tumor-associated antigen but also conferred strong oncogenic effects in HCC. Overexpression of CLDN6 induced phenotypic shift of HCC cells from hepatic lineage to biliary lineage, which was more refractory to sorafenib treatment. The enhanced tumor lineage plasticity and cellular identity change were potentially induced by the CLDN6/TJP2 (tight junction protein 2)/YAP1 (Yes-associated protein 1) interacting axis and further activation of the Hippo signaling pathway. A de novo anti-CLDN6 monoclonal antibody conjugated with cytotoxic agent (Mertansine) DM1 (CLDN6-DM1) was developed. Preclinical data on both HCC cell lines and primary tumors showed the potent antitumor efficiency of CLDN6-DM1 as a single agent or in combination with sorafenib in HCC treatment.


2020 ◽  
Vol 223 ◽  
pp. 33-43
Author(s):  
Yuwei Wu ◽  
Jinyu Wang ◽  
Xiaodong Zheng ◽  
Yongyan Chen ◽  
Mei Huang ◽  
...  

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