[Anti-angiogenesis of interferon-alpha2b in chronic myeloid leukemia in vitro].
This study was aimed to investigate the anti-angiogenesis of IFN-alpha2b in chronic myeloid leukemia (CML) in vitro by using K562 cell line and human umbilical vein endothelial cells (HUVEC). The levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) in culture supernatant of K562 cells were determined by ELISA; the expressions of VEGF and bFGF mRNA after treating K562 cells with 10(3), 10(2) and 10 U/ml IFN-alpha2b for 24, 36, 48 hours were detected by real-time RT-PCR; the effects of K562 cell culture supernatant and IFN-alpha2b on proliferation, migration and differentiation of HUVEC in vitro were assayed by MTT, Transwell chamber and tubule formation assay respectively. The results showed that the K562 cells expressed and secreted VEGF and bFGF. The culture supernatant of K562 cells significantly promoted the proliferation, migration and tubule formation of HUVEC in vitro in a concentration-dependent manner. After treating K562 cells with IFN-alpha2b 10 U/ml for 24, 36 and 48 hours, the expression levels of VEGF and bFGF mRNA were 1.64+/-0.18, 1.49+/-0.14, 1.31+/-0.05 and 1.53+/-0.10, 1.29+/-0.15, 0.79+/-0.13 respectively (p=0.002), but the expression levels of VEGF and bFGF mRNA were not significantly different along with increasing of IFN-alpha2b concentration. It is concluded that the angiogenesis exists in CML. The K562 cell expresses and secrets VEGF and bFGF, which promotes the proliferation, migration and differentiation of HUVEC. The IFN-alpha2b displays anti-angiogenesis by inhibiting the proliferation, migration and tubule formation in vitro of HUVEC and down regulating the expression of VEGF and bFGF mRNA.
Zhang
Li-Ming
LM
Department of Hematology, Jingzhou Central Hospital, Jingzhou 434020, Hubei Province, China.
Yu
Yong-Zhi
YZ
Huang
Zhi-Ping
ZP
Zhang
Wan-Sheng
WS
Dong
Li
L
D020533:Angiogenesis Inhibitors / Q000494:pharmacology*; D042783:Endothelial Cells / Q000187:drug effects*; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism; D006801:Humans; D000077190:Interferon alpha-2; D016898:Interferon-alpha / Q000494:pharmacology*; D020014:K562 Cells; D015464:Leukemia, Myelogenous, Chronic, BCR-ABL Positive / Q000378:metabolism / Q000473:pathology*; D009389:Neovascularization, Pathologic; D011994:Recombinant Proteins; D014471:Umbilical Veins / Q000166:cytology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D020533:Angiogenesis Inhibitors; D000077190:Interferon alpha-2; D016898:Interferon-alpha; D011994:Recombinant Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D016222:Fibroblast Growth Factor 2