Suppression of Vascular Endothelial Growth Factor (VEGF) Expression by Targeting the Bcr-Abl Oncogene and Protein Tyrosine Kinase Activity in Bcr-Abl-positive Leukaemia Cells  

Oleh:

Li, L. ; Zhang, R. ; Fang, Z.Y. ; Chen, J.N. ; Zhu, Z.L.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Journal of International Medical Research vol. 37 no. 02 (Mar. 2009), page 426-437.
Topik: Vascular Endothelial Growth Factor; Protein Tyrosine Kinase

Ketersediaan

Perpustakaan FK Nomor Panggil: J11.K.2009.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

Lihat Detail Induk

Isi artikel

Studies have shown that vascular endothelial growth factor (VEGF), a major and potent inducer of angiogenesis, is directly triggered by the disease-related oncogene Bcr-Abl in Bcr-Abl-positive cells. In this study, inhibition of Bcr-Abl tyrosine kinase activity by imatinib significantly decreased VEGF expression in Bcr-Abl-positive K562 cells in vitro. Imatinib treatment in vivo of nude mice xenografted with K562 cells resulted in a significant reduction in tumour size and microvessel density compared with untreated tumours. In addition, interfering with Bcr-Abl oncogene expression with small interfering RNAs (siRNAs) not only induced a specific reduction of Bcr-Abl mRNA and protein expression, but also efficiently inhibited the expression of VEGF in K562 cells. Combined treatment with imatinib and Bcr-Abl-targeting siRNAs resulted in an enhanced effect on VEGF suppression in K562 cells. The combined application of Bcr-Abl-targeting siRNAs and imatinib may provide a potent novel therapeutic approach for chronic myeloid leukaemia.

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