Potential molecular mechanisms underlying the effect of arsenic on angiogenesis
- 31 Downloads
Arsenic is a potent chemotherapeutic drug that is applied as a treatment for cancer; it exerts its functions through multiple pathways, including angiogenesis inhibition. As angiogenesis is a critical component of the progression of many diseases, arsenic is a feasible treatment option for patients with other angiogenic diseases, including rheumatoid arthritis and psoriasis, among others. However, arsenic is also a well-known carcinogen, demonstrating a pro-angiogenesis effect. This review will focus on the dual effects of arsenic on neovascularization and the relevant mechanisms underlying these effects, aiming to provide a rational understanding of arsenic treatment. In particular, we expect to provide a comprehensive overview of the current knowledge of the mechanisms by which arsenic influences angiogenesis.
KeywordsArsenic trioxide Arsenite Cancer Angiogenesis Toxicity
This work is supported by National Natural Science Foundation of China (NSFC 81771749) to Zhiyi Zhang, Chinese Postdoctoral Science Foundation (Grant No. 2019M651309) to Juan Zhang, Heilongjiang Provincial Postdoctoral Science Foundation (Grant No. LBH-Z18226) to Juan Zhang, and Scientific Research Innovation Foundation of the First Affiliated Hospital of Harbin Medical University (Grant No. 2019B18) to Juan Zhang.
Compliance with ethical standards
Conflict of interest
The authors declare that there is no conflict of interest.
- Chung I, Han G, Seshadri M, Gillard BM, Yu WD (2009) Role of vitamin D receptor in the antiproliferative effects of calcitriol in tumor-derived endothelial cells and tumor angiogenesis in vivo. Cancer Res 69:967–975. https://doi.org/10.1158/0008-5472.CAN-08-2307 CrossRefPubMedPubMedCentralGoogle Scholar
- Duyndam MC, Hulscher ST, van der Wall E, Pinedo HM, Boven E (2003) Evidence for a role of p38 kinase in hypoxia-inducible factor 1-independent induction of vascular endothelial growth factor expression by sodium arsenite. J Biol Chem 278:6885–6895. https://doi.org/10.1074/jbc.M206320200 CrossRefPubMedGoogle Scholar
- Hei TK, Filipic M (2004) Role of oxidative damage in the genotoxicity of arsenic. Free Radic Biol Med 37:574–581. https://doi.org/10.1016/j.freeradbiomed.2004.02.003 CrossRefPubMedGoogle Scholar
- Mohammadi Kian M, Mohammadi S, Tavallaei M, Chahardouli B, Rostami S (2018) Inhibitory effects of arsenic trioxide and thalidomide on angiogenesis and vascular endothelial growth factor expression in leukemia cells. Asian Pac J Cancer Prev 19:1127–1134. https://doi.org/10.22034/APJCP.2018.19.4.1127 CrossRefPubMedGoogle Scholar
- Sun H, Ma L, Hu Z (1992) Arsenic trioxide treated 32 cases of acute promyelocytic leukemia. Chin J Integr Tradit West Med 12:170–172Google Scholar
- Tomanek RJ, Schatteman GC (2000) Angiogenesis: new insights and therapeutic potential. Anat Rec 261:126–135. https://doi.org/10.1002/1097-0185(20000615)261:33.0.CO;2-4 CrossRefPubMedGoogle Scholar
- Xiao YF, Wu DD, Liu SX, Chen X, Ren LF (2007) Effect of arsenic trioxide on vascular endothelial cell proliferation and expression of vascular endothelial growth factor receptors Flt-1 and KDR in gastric cancer in nude mice. World J Gastroenterol 13:6498–6505. https://doi.org/10.3748/wjg.13.6498 CrossRefPubMedPubMedCentralGoogle Scholar