We have located links that may give you full text access.
Interaction of EZH2 and P65 is involved in the arsenic trioxide-induced anti-angiogenesis in human triple-negative breast cancer cells.
Cell Biology and Toxicology 2019 January 6
Breast cancer (BC) is the most common female malignancy in the world. Triple-negative breast cancer (TNBC) is a subtype of BC characterized by the lack of estrogen receptors, progesterone receptors, and human epidermal growth factor receptor-2 (HER-2), resulting in the limited therapeutic options. Due to the aggressive behaviors at early stage, TNBC exhibits poorer outcomes compared to other BC subtypes. Hematogenous metastasis, which spreads cancerous cells to lungs and/or bones, plays a pivotal role in the progression of TNBC. Therefore, it is of great importance to study the anti-angiogenesis regulation mechanism for finding new treatment options for TNBC. Arsenic trioxide (ATO) exhibits anti-cancer effect on solid tumors, including TNBC. However, the roles and the molecular mechanism of ATO in the anti-angiogenesis of TNBC remain less well documented. Our data showed that ATO restrained the expression and secretion of vascular endothelial growth factor (VEGF) and impaired the angiogenic ability in TNBC cells. In addition, ATO suppressed the angiogenic ability in TNBC by inhibiting the interaction of the enhancer of zeste homolog 2 (EZH2) with p65, downregulating the nuclear factor-κB (NF-κB) activity, hence contributing to the regulation of IL-6/Stat3 signaling pathway. All of our findings would help to better understand the mechanism of ATO anti-angiogenesis in TNBC, thus highlighting the therapeutic potential of ATO in TNBC by targeting angiogenesis.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app