Abstract
We have analyzed the role of cocaine in the control of the rat fibroblast (EL2) cell proliferation. Our data show a dose-related effect on the inhibition of DNA synthesis and cell growth when cocaine is added with serum or with a pure growth factor [Epidermal Growth Factor (EGF)]. Pretreatment by drug did not appreciably enhance the inhibition of S-phase entry above that obtained when cocaine and mitogen were added simultaneously. On the contrary, exposure of quiescent EL2 cells to cocaine has little or no effect on DNA synthesis, when drug is removed before the mitogenic stimulus. Moreover, even when cocaine is added after EGF, an exposure only within 1-8 hours is required in order to inhibit stimulation of DNA synthesis. Cocaine also suppressed the general increase in protein synthesis that occurs during the first hour after EGF addition. The combined data suggest that cocaine inhibits the traverse of mitogen-stimulated quiescent EL2 cells from Go to S phase by acting on processes that take place during the initial phase of the cell cycle.
| Original language | English |
|---|---|
| Pages (from-to) | 549-558 |
| Number of pages | 10 |
| Journal | Cell Biology International Reports |
| Volume | 14 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - 1990 |
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ASJC Scopus subject areas
- Cell Biology
Cite this
Inhibition of rat fibroblast cell proliferation at specific cell cycle stages by cocaine. / Di Francesco, Paolo; Pica, Francesca; Favalli, Cartesio; Tubaro, Ezio; Garaci, Enrico.
In: Cell Biology International Reports, Vol. 14, No. 6, 1990, p. 549-558.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Inhibition of rat fibroblast cell proliferation at specific cell cycle stages by cocaine
AU - Di Francesco, Paolo
AU - Pica, Francesca
AU - Favalli, Cartesio
AU - Tubaro, Ezio
AU - Garaci, Enrico
PY - 1990
Y1 - 1990
N2 - We have analyzed the role of cocaine in the control of the rat fibroblast (EL2) cell proliferation. Our data show a dose-related effect on the inhibition of DNA synthesis and cell growth when cocaine is added with serum or with a pure growth factor [Epidermal Growth Factor (EGF)]. Pretreatment by drug did not appreciably enhance the inhibition of S-phase entry above that obtained when cocaine and mitogen were added simultaneously. On the contrary, exposure of quiescent EL2 cells to cocaine has little or no effect on DNA synthesis, when drug is removed before the mitogenic stimulus. Moreover, even when cocaine is added after EGF, an exposure only within 1-8 hours is required in order to inhibit stimulation of DNA synthesis. Cocaine also suppressed the general increase in protein synthesis that occurs during the first hour after EGF addition. The combined data suggest that cocaine inhibits the traverse of mitogen-stimulated quiescent EL2 cells from Go to S phase by acting on processes that take place during the initial phase of the cell cycle.
AB - We have analyzed the role of cocaine in the control of the rat fibroblast (EL2) cell proliferation. Our data show a dose-related effect on the inhibition of DNA synthesis and cell growth when cocaine is added with serum or with a pure growth factor [Epidermal Growth Factor (EGF)]. Pretreatment by drug did not appreciably enhance the inhibition of S-phase entry above that obtained when cocaine and mitogen were added simultaneously. On the contrary, exposure of quiescent EL2 cells to cocaine has little or no effect on DNA synthesis, when drug is removed before the mitogenic stimulus. Moreover, even when cocaine is added after EGF, an exposure only within 1-8 hours is required in order to inhibit stimulation of DNA synthesis. Cocaine also suppressed the general increase in protein synthesis that occurs during the first hour after EGF addition. The combined data suggest that cocaine inhibits the traverse of mitogen-stimulated quiescent EL2 cells from Go to S phase by acting on processes that take place during the initial phase of the cell cycle.
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UR - http://www.scopus.com/inward/citedby.url?scp=0025371520&partnerID=8YFLogxK
U2 - 10.1016/0309-1651(90)91182-4
DO - 10.1016/0309-1651(90)91182-4
M3 - Article
C2 - 2369763
AN - SCOPUS:0025371520
VL - 14
SP - 549
EP - 558
JO - Cell Biology International Reports
JF - Cell Biology International Reports
SN - 0309-1651
IS - 6
ER -