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Young S. Yu, Jang Won Heo, Hyoung Oh Jun, Jin Hyoung Kim, Kyu-Won Kim, Jeong Hun Kim; Inhibitory Activity of Bevacizumab to Differentiation of Retinoblastoma Cells through Blockade of ERK Pathway. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2250.
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To investigate whether bevacizumab as an anti-VEGF antibody could inhibit differentiation of retinoblastoma cells without affection to cellular viability, which would be mediated via blockade of extracellular signal-regulated kinase (ERK) 1/2 activation.
Human retinoblastoma cells, SNUOT-Rb1, were differentiated by treatment of 0.1% bovine serum albumin (BSA), and then treated by anti-VEGF antibody (Bevacizumab) for 48 hours. To determine the effect of bevacizumab on differentiation of SNUOT-Rb1, neurofilament and Shank 2 were detected by Western blot analysis and immunocytochemistry. Furthermore, extracellular signal-regulated kinases 1 and 2 (ERK 1/2) phosphorylation was also detected.
The retinoblastoma cells expressed VEGFR-2 as well as TrkA which is a neurotrophin receptor associated with differentiation of retinoblastoma cells. TrkA in retinoblastoma cells was activated with VEGF treatment. Interestingly even in the concentration of no cellular death, bevascizumab significantly attenuated the neurite formation of differentiated retinoblastoma cells, which was accompanied by inhibition of neurofilament and shank2 expression. Furthermore, bevacizumab inhibited differentiation of retinoblastoma cells by blockade of ERK 1/2 activation.
Based on that the differentiated retinoblastoma cells are mostly photoreceptors, our results suggest that anti-VEGF therapies would affect to the maintenance or function of photoreceptors in mature retina.
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