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TAD1822-7 induces ROS-mediated apoptosis of HER2 positive breast cancer by decreasing E-cadherin in an EphB4 dependent manner

Published:15 November 2021 DOI: 10.1016/j.lfs.2021.119954 PMID: 34520770
Man Zhu, Xiaoyu Tang, Zhengyan Gong, Wenjuan Tang, Yanmin Zhang

Abstract

HER2-positive breast cancer (HER2-BC) shows the over-expression of tyrosine kinase receptor EphB4 associated with poor disease prognosis. E-cadherin is found as a survival factor in multiple models of breast cancer by suppressing reactive oxygen-mediated apoptosis. This study confirmed that both HER2 and EphB4 are positively correlated with E-cadherin in HER2-BC. Inhibition of HER2 or EphB4 is discovered to induce ROS-dependent apoptosis by decreasing E-cadherin expression in SKBR3 and MDA-MB-453 cells. TAD1822-7 (TAD), a novel biphenyl urea taspine derivative, exhibits good growth inhibition, apoptosis induction and ROS accumulation effects on SKBR3 and MDA-MB-453 cells. Mechanistic investigation revealed that TAD blockades both EphB4 positive signal transduction and activation of HER2 signal transduction, thereby suppressing E-cadherin/TGF-β/p-Smad2/3 signaling axis to elicit ROS-dependent endogenous mitochondrial apoptosis. Together, these findings not only provide a new approach for HER2-BC therapy but also increase our understanding of the regulating effect of E-cadherin by HER2 and EphB4 in ROS-mediated apoptosis.

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Procduct Name CAS Molecular Formula Supplier Price
N-Acetyl-L-cysteine 616-91-1 C5H9NO3S 1337 suppliers $5.00-$3143.10
N-Acetyl-L-cysteine 616-91-1 C5H9NO3S 1337 suppliers $5.00-$3143.10
N-Acetyl-L-cysteine 616-91-1 C5H9NO3S 1337 suppliers $5.00-$3143.10
N-Acetyl-L-cysteine 616-91-1 C5H9NO3S 1337 suppliers $5.00-$3143.10
LY 2157299 700874-72-2 C22H19N5O 263 suppliers $13.00-$2822.00
LY 2157299 700874-72-2 C22H19N5O 263 suppliers $13.00-$2822.00
LY 2157299 700874-72-2 C22H19N5O 263 suppliers $13.00-$2822.00
LY 2157299 700874-72-2 C22H19N5O 263 suppliers $13.00-$2822.00
N-Acetyl-L-cysteine 616-91-1 - Inquiry
N-Acetyl-L-cysteine 616-91-1 - Inquiry

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