Genetics and Molecular Biology Research Unit - UPGEM, Medical School of Sao Jose do Rio Preto - FAMERP, Av. Brigadeiro Faria Lima, 5416, Bloco U6, Sao Jose do Rio Preto, SP 15090-000, Brazil.
J Cancer Res Clin Oncol. 2012 Mar;138(3):363-70. doi: 10.1007/s00432-011-1073-2. Epub 2011 Nov 2.
Tumor growth and progression depend on angiogenesis, a process of new blood vessels formation from a preexisting vascular endothelium. Tumors promote angiogenesis by secreting or activating angiogenic factors that stimulate endothelial proliferation and migration and capillary morphogenesis. The newly formed blood vessels provide nutrients and oxygen to the tumor, increasing its growth. Thus, angiogenesis plays a key role in cancer progression and development of metastases. An important growth factor that promotes angiogenesis and participates in a variety of physiological and pathological processes is the vascular endothelial growth factor (VEGF-A or VEGF). Overexpression of VEGF results in increased angiogenesis in normal and pathological conditions. The existence of an alternative site of splicing at the 3' untranslated region of the mRNA results in the expression of isoforms with a C-terminal region which are downregulated in tumors and may have differential inhibitory effects. This suggests that control of splicing can be an important regulatory mechanism of angiogenesis in cancer.
肿瘤的生长和进展依赖于血管生成，即从预先存在的血管内皮细胞形成新的血管的过程。肿瘤通过分泌或激活血管生成因子来促进血管生成，这些因子刺激内皮细胞增殖、迁移和毛细血管形态发生。新形成的血管为肿瘤提供营养和氧气，从而促进其生长。因此，血管生成在癌症的进展和转移的发展中起着关键作用。一种促进血管生成并参与各种生理和病理过程的重要生长因子是血管内皮生长因子（VEGF-A 或 VEGF）。VEGF 的过度表达导致正常和病理条件下血管生成增加。在 mRNA 的 3'非翻译区存在剪接的替代位点，导致表达具有 C 末端区域的异构体，这些异构体在肿瘤中下调，并且可能具有不同的抑制作用。这表明剪接的控制可能是癌症中血管生成的重要调节机制。
