Inhibitory Effects of Arsenic Trioxide and Thalidomide on Angiogenesis and Vascular Endothelial Growth Factor Expression in Leukemia Cells
| Autor: | Mohammadi Kian M; Hematology Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran.Email: m-nikbakht@sina.tums.ac.ir, smohammadi@sina.tums.ac.ir, Mohammadi S, Tavallaei M, Chahardouli B, Rostami S, Zahedpanah M, Ghavamzadeh A, Nikbakht M |
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| Jazyk: | angličtina |
| Zdroj: | Asian Pacific journal of cancer prevention : APJCP [Asian Pac J Cancer Prev] 2018 Apr 27; Vol. 19 (4), pp. 1127-1134. Date of Electronic Publication: 2018 Apr 27. |
| DOI: | 10.22034/APJCP.2018.19.4.1127 |
| Abstrakt: | Acute myeloid leukemia (AML) is a blood disorder characterized by uncontrolled proliferation of myeloid progenitors and decrease in the apoptosis rate. The vascular endothelial growth factor (VEGF) promotes blood vessel regeneration which might play important roles in development and progression of neoplasia. Our previous studies focused on cytotoxicity and anticancer effects of arsenic trioxide (ATO) and thalidomide (THAL) as an anti-VEGF compound in the AML cell model. ATO also affects regulatory genes involved in cell proliferation and apoptosis. The aim of present study was to examine the effects of ATO and THAL alone and in combination on U937 and KG-1 cells , with attention to mRNA expression for VEGF isoforms. Growth inhibitory effects was assessed by MTT assay and apoptosis induction was determined by Annexin/PI staining. mRNA expression levels were evaluated by real-time PCR. Our data indicated that ATO (1.618μM and 1μM in KG-1 and U937 cell lines respectively), THAL (80μM and 60μM) and their combination inhibited proliferation and induced apoptosis in our cell lines. mRNA expression of VEGF (A, B) decreased while C and D isoforms did not show any significant changes. Taken together, according to the obtained results, the VEGF autocrine loop could be a target as a therapeutic strategy for cases of AML. (Creative Commons Attribution License) |
| Databáze: | MEDLINE |
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