Differentiation of Y79 retinoblastoma cells induced by succinylated concanavalin A.

Abstract

The growth and differentiation potential of Y79 human retinoblastoma cells was assessed in vitro following treatment with the differentiating agent succinylated concanavalin A (SCA). Since SCA treatment induced Y79 cells to display differentiated morphologies in vitro, we sought to determine potential differentiated phenotypes with the use of retinal cell markers. Seventy-two h after SCA treatment, Y79 cells exhibited a decrease in the glial cell marker GFAP and a dramatic and reversible increase in the photoreceptor marker IRBP, while maintaining neuron-specific enolase and PGP 9.5 positivity. These results were indicative of a predominantly neuronal, photoreceptor cell population in response to SCA treatment. In addition, Y79 cell growth inhibition was observed in response to SCA, which could be reversed within 24 h of treatment with the blocking sugar alpha-methyl-D-mannoside. These changes were accompanied by a significant modulation of the N-MYC oncoprotein, as detected by Western blot analysis and immunocytochemistry. Thus, in this system, the status of N-MYC seems to be closely linked to changes in the growth and differentiated state of SCA-treated Y79 retinoblastoma cells.

• Authors: G M Seigel, M F Notter
• Journal: Cell growth & differentiation : the molecular biology journal of the American Association for Cancer Research (Cell Growth Differ) Vol. 4 Issue 1 Pg. 1-7 (Jan 1993) ISSN: 1044-9523 [Print] United States
• PMID: 8424902 (Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Eye Proteins
• Proto-Oncogene Proteins c-myc
• Retinol-Binding Proteins
• interstitial retinol-binding protein
• Concanavalin A
• succinylconcanavalin A

Topics

• Cell Differentiation (drug effects)
• Cell Division (drug effects)
• Concanavalin A (therapeutic use)
• Eye Proteins (biosynthesis)
• Humans
• Mitotic Index
• Neuroglia (drug effects)
• Neurons (drug effects)
• Phenotype
• Proto-Oncogene Proteins c-myc (biosynthesis)
• Retinoblastoma (drug therapy, metabolism, pathology)
• Retinol-Binding Proteins (biosynthesis)
• Tumor Cells, Cultured