The relationship between cell morphology, suramin and lysyl oxidase mRNA
Date
1999
DOI
Authors
Gross, Howard
Version
OA Version
Citation
Abstract
Suramin is an anticancer drug that normalizes the phenotype of some transformed cells. Preliminary studies show that suramin increases lysyl oxidase mRNA levels and causes phenotypic reversion of c-H-ras transformed NIH3T3 cells (RS485 cell line). Lysyl oxidase is an extracellular enzyme that catalyzes the final step for cross-linking and insolubilization of collagen and elastin in the extracellular matrix. It has been shown to act as a tumor suppressor.
The purpose of this study was to determine whether the increase in lysyl oxidase mRNA levels is key to suramin’s effect on the phenotype of RS485 cells.
This was accomplished by transfection of RS485 with an antisense lysyl oxidase expression vector and with empty vector (PCDNA3) followed by Southern blot and Northern blot analyses after suramin treatment of cells. Results show that two antisense clones (As 8, As 14) remain refractile in the presence of suramin while lysyl oxidase mRNA levels remain low, and control as pc16 and RS485 change morphology from refractile to flat while lysyl oxidase mRNA were increased.
These results and other preliminary studies showing that suramin inhibits lysyl oxidase enzyme activity, suggest that lysyl oxidase mRNA in some way maintains normal cell phenotype. Further research should be done on cell kinetics, growth rate and morphology of these clones, grown in the presence and absence of suramin.
Description
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Thesis (M.Sc.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 1999 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 25-28).
Thesis (M.Sc.D.)--Boston University, Henry M. Goldman School of Dental Medicine, 1999 (Periodontology and Oral Biology).
Includes bibliographical references (leaves 25-28).
License
This work is protected by copyright. Downloading is restricted to the BU community. If you are the author of this work and would like to make it publicly available, please contact open-help@bu.edu.