Expression of c-myc and induction of DNA synthesis by platelet-poor plasma in human diploid fibroblasts

Ferrari, Sérgio; Calabretta, Bruno; Battini, Renata; Cosenza, Stephen C.; Owen, Thomas A.; Soprano, Kenneth J.; Baserga, Renato

doi:10.1016/0014-4827(88)90138-3

Cited by 18 publications

(10 citation statements)

References 28 publications

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“…This same group (Kaczmarek et al, 1986) also showed that elevation of c-myc mRNA by cycloheximide treatment could replace the requirement for PDGF and allow 3T3 cells to enter S phase in platelet-poor plasma alone. These observations in 3T3 cells are consistent with our own report showing that WI-38 cells growth arrested for less than 15 days contained high levels of c-myc and could be stimulated with plasma alone, whereas 20 day growth-arrested cells, which have lower levels of c-myc (and several other growth-associated gene transcripts), required full serum (Ferrari et al, 1988). Finally, Kelekar and Cole (1987) showed that introduction and constitutive expression of either c-myc, activated c-Ha-ras, or adenovirus E l a in baby rat kidney cells considerably altered the growth factor responsiveness of the resulting cell lines.…”

Section: Discussionsupporting

confidence: 92%

Analysis of the growth factor requirements for stimulation of WI‐38 cells after extended periods of density‐dependent growth arrest

Owen

Soprano

1989

Journal Cellular Physiology

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When cultures of WI-38 human diploid fibroblasts reach high cell densities, they cease to proliferate and enter a viable state of quiescence. WI-38 cells can remain in this quiescent state for long periods of time; however, the longer the cells remain growth arrested, the more time they require to leave G0, progress through G1, and enter S after stimulation with fresh serum. The experiments presented here compare the response of long-term quiescent WI-38 cells (stimulated 26 days after plating) and short-term quiescent WI-38 cells (stimulated 12 days after plating) to treatment with a variety of individual purified growth factors instead of whole serum. Our results show that the qualitative and quantitative growth factor requirements necessary to stimulate G1 progression and entry into S were the same for both short- and long-term quiescent WI-38 cells, in that the same defined medium (supplemented with epidermal growth factor [EGF], recombinant human insulin-like growth factor 1 [IGF-1], and dexamethasone [DEX]) stimulated both populations of cells to proliferate with the same kinetics and to the same extent as serum. However, the long-term quiescent WI-38 cells were found to exhibit a difference in the time during which either serum or these individual growth factors were required to be present during the prereplicative period. We believe that this difference may be the cause of the prolongation of the prereplicative phase after stimulation of long-term density-arrested WI-38 cells.

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Section: Discussionsupporting

confidence: 92%

Analysis of the growth factor requirements for stimulation of WI‐38 cells after extended periods of density‐dependent growth arrest

Owen

Soprano

1989

Journal Cellular Physiology

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“…The results reported above may be related to Ferrari et al's (12) report, in which unexpected differences between growth fraction and cell sensitivity to progression factors is described. He reported that, in WI-38 human fibroblast culture, 7 days after reaching confluence (GF determined by L3H1thymidine continuous labeling), cells remained sensitive to platelet-poor plasma (PPP), which contains a progression factor.…”

Section: Discrepancies Between Progression Growth Factor Sensitivity supporting

confidence: 67%

Ki‐67 labeling in postmitotic cells defines different Ki‐67 pathways within the 2c compartment

Manoir

Guillaud²,

Camus

et al. 1991

Cytometry

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Simultaneous quantification of DNA and Ki-67 proliferation-associated antigen was performed using fluorescence image cytometry. In the MCF-7 cell line, the Ki-67 antigen content increases during the cell cycle, and its intranuclear distribution pattern varies. Quantitative evolution of Ki-67 content as a function of nuclear area makes it possible to define several pathways followed by cells going through the 2c compartment. 1) In some cells, the amount of Ki-67 antigen remains constant during G1 (Ki-67 stable pathway), and a characteristic speckled pattern can be observed. 2) In the larger fraction of cells analyzed, there is a postmitotic decrease in the Ki-67 (Ki-67 decrease pathway) content. In this pathway, labeling is located in the nucleoplasm in small nuclei, is located in nucleoli in intermediate-sized nuclei, and is absent from larger nuclei (G0). A progressive increase in Ki-67 content (Ki-67 increase pathway) was observed from intermediate-sized nuclei to S phase nuclei. From these results, we hypothesize that the Ki-67 stable pathway is the G1 phase of newly formed cells going directly to S phase in local optimal conditions of growth and that Ki-67 decrease pathway and Ki-67 increase pathway correspond to cells whose progression to S phase is regulated by extracellular factors.

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“…Previous studies from our laboratory have already shown that basal levels of c-Myc mRNA are maintained in short-term quiescent WI-38 cells but are reduced to below levels of detection (by RNAse protection) in long-term quiescent cells (Ferrari et al, 1988). In contrast, Max mRNA and protein levels have been shown to be extremely stable in a number of model systems Blackwood et al, 1992;Blackwood and Eisenman, 1991;Prendergast et al, 1991;Wagner et al, 1992).…”

Section: Discussionmentioning

confidence: 93%

Regulation of human ornithine decarboxylase expression following prolonged quiescence: Role for the c‐Myc/Max protein complex

Peña

Hickok

et al. 1995

Journal Cellular Physiology

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WI-38 cells can remain quiescent for long periods of time and still be induced to reenter the cell cycle by the addition of fresh serum. However, the longer these cells remain growth arrested, the more time they require to enter S phase. This prolongation of the prereplicative phase has been localized to a point early in G1, after the induction of "immediate early" G1 genes such as c-fos and c-jun but before maximal expression of "early" G1 genes such as ornithine decarboxylase (ODC). Understanding the molecular basis for ODC mRNA induction can therefore provide information about the molecular events which regulate the progression of cells out of long-term quiescence into G1 and subsequently into DNA synthesis. Studies utilizing electrophoretic mobility shift assays (EMSA) of nuclear extracts from short- and long-term quiescent WI-38 cells identified a region of the human ODC promoter at -491 bp to -474 bp which exhibited a protein binding pattern that correlated with the temporal pattern of ODC mRNA expression. The presence of a CACGTG element within this fragment, studies with antibodies against c-Myc and Max, the use of purified recombinant c-Myc protein in the mobility shift assay, and antisense studies suggest that these proteins can specifically bind this portion of the human ODC promoter in a manner consistent with growth-associated modulation of the expression of ODC and other early G1 genes following prolonged quiescence. These studies suggest a role for the c-Myc/Max protein complex in regulating events involved in the progression of cells out of long-term quiescence into G1 and subsequently into S.

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Expression of c-myc and induction of DNA synthesis by platelet-poor plasma in human diploid fibroblasts

Cited by 18 publications

References 28 publications

Analysis of the growth factor requirements for stimulation of WI‐38 cells after extended periods of density‐dependent growth arrest

Analysis of the growth factor requirements for stimulation of WI‐38 cells after extended periods of density‐dependent growth arrest

Ki‐67 labeling in postmitotic cells defines different Ki‐67 pathways within the 2c compartment

Regulation of human ornithine decarboxylase expression following prolonged quiescence: Role for the c‐Myc/Max protein complex

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