Corpus ID: 6999198

Vascular endothelial growth factor inhibits apoptotic death in hematopoietic cells after exposure to chemotherapeutic drugs by inducing MCL1 acting as an antiapoptotic factor.

  title={Vascular endothelial growth factor inhibits apoptotic death in hematopoietic cells after exposure to chemotherapeutic drugs by inducing MCL1 acting as an antiapoptotic factor.},
  author={O Katoh and Toshitada Takahashi and Tetsuya Oguri and Ken Kuramoto and Keiichiro Mihara and M. Kobayashi and Shitau Hirata and Hideomi Watanabe},
  journal={Cancer research},
  volume={58 23},
We reported previously that vascular endothelial growth factor (VEGF) inhibits the apoptotic death of hematopoietic cells that is induced by exposure to ionizing radiation (O. Katoh et al., Cancer Res., 55: 5687-5692, 1995). In this study, we show that VEGF also inhibits apoptotic cell death that is induced by exposure to the chemotherapeutic drugs etoposide and doxorubicin. To elucidate the molecular mechanisms underlying this inhibitory effect of VEGF, we examined expression levels of BCL2… Expand
VEGF(165) promotes survival of leukemic cells by Hsp90-mediated induction of Bcl-2 expression and apoptosis inhibition.
It is demonstrated that Hsp90 mediates antiapoptotic and survival-promoting effects of V EGF, which may contribute to the survival advantage of VEGFR(+) cells such as subsets of leukemias. Expand
Vascular endothelial growth factor (VEGF) upregulates BCL-2 and inhibits apoptosis in human and murine mammary adenocarcinoma cells
VEGF resulted in reduced tumour cell apoptosis, whereas its inhibition with anti-VEGF neutralizing antibodies induced apoptosis directly in tumour cells, therefore, in addition to its role in angiogenesis and vessel permeability, VEGF acts as a survival factor for tumours, inducing Bcl-2 expression and inhibiting tumours apoptosis. Expand
Hematopoietic Cells Endothelial Growth Factor and Inhibits Apoptotic Death in a Novel Zinc Finger Gene , Is Induced by Vascular
Vascular endothelial growth factor (VEGF) inhibits radiation-induced apoptosis in the leukemia cell line, CMK86 (O. Katohet al.,Cancer Res., 55: 5687–5692, 1995). To elucidate the molecularExpand
Targeted inhibition of VEGF-modulated survival and arsenic sensitivity in acute myeloid leukemia (AML)
Target inhibition of VEGF suppressed survival and increased arsenic sensitivity in AML and showed synergistic inhibitory effects between AS and ATO. Expand
The protein tyrosine kinase inhibitor SU5614 inhibits VEGF-induced endothelial cell sprouting and induces growth arrest and apoptosis by inhibition of c-kit in AML cells.
The data provide strong evidence that SU5614 has a dual mode of action, and by direct inhibition of c-Kit in AML cells and by inhibition of VEGFR-2 in endothelial cells, it might represent a novel treatment option for patients with c-kit+ AML. Expand
VEGF-induced phosphorylation of Bcl-2 influences B lineage leukemic cell response to apoptotic stimuli
It is demonstrated that Bcl-2 was constitutively phosphorylated in several hematopoietic tumor cell lines and in primary ALL cells, suggesting that optimal protection of leukemic cells by VEGF may require activation of a pathway that includes B cl-2 phosphorylation. Expand
Hepatocyte growth factor-activated NF-κB regulates HIF-1 activity and ODC expression, implicated in survival, differently in different carcinoma cell lines
By regulating HIF-1 activity and specific gene expression downstream, NF-kappaB may influence the survival threshold, with an impact on the fate of carcinoma cells after prolonged HGF treatment. Expand
Effects of autocrine vascular endothelial growth factor (VEGF) in non-small cell lung cancer cell line A549
The data indicate that VEGF expression is efficiently inhibited in A549 cells by ASODN transfection and this inhibition leads to inhibited cell growth and impaired cell cycle distribution. Expand
VEGF induces Mcl-1 up-regulation and protects multiple myeloma cells against apoptosis.
It is demonstrated that deletion of Mcl-1 reduces fetal bovine serum (FBS)-, VEGF-, and IL-6-induced proliferation and protection of MM patient cells against FBS starvation-induced apoptosis, providing the preclinical framework for novel therapeutics targeting M cl-1 and/or V EGF to improve patient outcome in MM. Expand
In vivo administration of vascular endothelial growth factor (VEGF) and its antagonist, soluble neuropilin-1, predicts a role of VEGF in the progression of acute myeloid leukemia in vivo.
Results demonstrate that angiogenic factors such as VEGF promote AML progression in vivo and offer a potential treatment for AML, and a novel in vivo drug delivery model may be useful for testing the activities of other peptide antiangiogenic Factors. Expand