Open AccessThe cell cycle dependence of c‐sis gene expression: artifactual conclusions in cells prepared by chemical but not physical techniques
Author(s) -
Press R. D.,
Jacobberger J. W.,
Samols D.,
Goldthwait D.
Publication year - 1990
Publication title -
cell proliferation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.647
H-Index - 74
eISSN - 1365-2184
pISSN - 0960-7722
DOI - 10.1111/j.1365-2184.1990.tb01126.x
Subject(s) - cell cycle , rna , autocrine signalling , cell , biology , gene expression , platelet derived growth factor receptor , microbiology and biotechnology , cell growth , aphidicolin , dna synthesis , gene , dna , growth factor , receptor , biochemistry
. The c‐sis oncogene encoding the B‐chain of platelet‐derived growth factor (PDGF) may be involved in an autocrine growth stimulation of tumours expressing the PDGF receptor, such as glioblastomas and sarcomas. To investigate whether expression of c‐sis RNA is regulated in a cell cycle dependent manner, human A172 glioblastoma cells were synchronized by either centrifugal elutriation or chemical blockage with the DNA synthesis inhibitors hydroxyurea or aphidicolin. In non‐perturbed elutriated cells, c‐sis RNA levels were lower in the S phase of the cell cycle than in the G 1 phase. In contrast, the chemically synchronized cells revealed a transient rise in c‐sis RNA shortly after drug release, in early S phase. The RNA changes occurring after release from drug inhibition represent cell recovery from drug induced metabolic disturbances rather than true cell cycle dependent effects.