BIPHASIC EFFECT OF ADENOSINE ON CELL GROWTH AND CELL CYCLE OF HUMAN LYMPHOID CELL LINES: 219

We determined the effect of cell cycle position on the amount of dexamethasone that was specifically bound by mouse and human lymphoid cell lines. Cell lines that were either sensitive or resistant to growth inhibition by dexamethasone were compared. Exponentially growing cells were separated by centrifugal elutriation into fractions that corresponded to different positions in the cell cycle. The cell cycle phase distribution of each fraction was estimated by flow cytometry and autoradiography. The amount of dexamethasone bound per cell in each fraction was measured by a whole cell binding assay. In three dexamethasone-sensitive cell lines (two mouse and one human), we found that the amount of dexamethasone bound per cell increased 2–4-fold between G1 phase and S phase, and then decreased during G2/M phase. Results were the same when the amount of dexamethasone bound per milligram of cell protein was measured. Binding affinity was the same during G1 phase and S phase, but the proportion of bound dexamethasone that translocated to the nucleus was greater during S phase. In contrast, we found that the amount of dexamethasone bound per cell by three dexamethasone-resistant cell lines (two mouse and one human) did not increase during S phase. Our results indicate that cell cycle changes in dexamethasone binding are not simply related to changes in cell protein or cell volume during the cell cycle. An increase in dexamethasone binding during S phase may be required for dexamethasone to inhibit cell growth, and a failure of dexamethasone binding to increase during S phase might represent a new mechanism of dexamethasone resistance in lymphoid cells.

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Effect of cell cycle position on dexamethasone binding by mouse and human lymphoid cell lines: correlation between an increase in dexamethasone binding during S phase and dexamethasone sensitivity

Blood ◽

10.1182/blood.v63.1.105.105 ◽

1984 ◽

Vol 63 (1) ◽

pp. 105-113 ◽

Cited By ~ 16

Author(s):

CW Distelhorst ◽

BM Benutto ◽

RA Bergamini

Keyword(s):

Cell Cycle ◽

Cell Lines ◽

Lymphoid Cell ◽

S Phase ◽

Lymphoid Cells ◽

Cell Protein ◽

G1 Phase ◽

Cycle Phase ◽

Human Lymphoid Cell ◽

Lymphoid Cell Lines

Abstract We determined the effect of cell cycle position on the amount of dexamethasone that was specifically bound by mouse and human lymphoid cell lines. Cell lines that were either sensitive or resistant to growth inhibition by dexamethasone were compared. Exponentially growing cells were separated by centrifugal elutriation into fractions that corresponded to different positions in the cell cycle. The cell cycle phase distribution of each fraction was estimated by flow cytometry and autoradiography. The amount of dexamethasone bound per cell in each fraction was measured by a whole cell binding assay. In three dexamethasone-sensitive cell lines (two mouse and one human), we found that the amount of dexamethasone bound per cell increased 2–4-fold between G1 phase and S phase, and then decreased during G2/M phase. Results were the same when the amount of dexamethasone bound per milligram of cell protein was measured. Binding affinity was the same during G1 phase and S phase, but the proportion of bound dexamethasone that translocated to the nucleus was greater during S phase. In contrast, we found that the amount of dexamethasone bound per cell by three dexamethasone-resistant cell lines (two mouse and one human) did not increase during S phase. Our results indicate that cell cycle changes in dexamethasone binding are not simply related to changes in cell protein or cell volume during the cell cycle. An increase in dexamethasone binding during S phase may be required for dexamethasone to inhibit cell growth, and a failure of dexamethasone binding to increase during S phase might represent a new mechanism of dexamethasone resistance in lymphoid cells.

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Reversible G1 arrest in the cell cycle of human lymphoid cell lines by dimethyl sulfoxide

Experimental Cell Research ◽

10.1016/0014-4827(90)90108-m ◽

1990 ◽

Vol 187 (1) ◽

pp. 4-10 ◽

Cited By ~ 42

Author(s):

Masaji Sawai ◽

Kozo Takase ◽

Hirobumi Teraoka ◽

Kinji Tsukada

Keyword(s):

Cell Cycle ◽

Dimethyl Sulfoxide ◽

Cell Lines ◽

Lymphoid Cell ◽

G1 Arrest ◽

Human Lymphoid Cell ◽

Lymphoid Cell Lines

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Human Lymphoid Cell Lines in Biochemical Genetics

Pediatrics International ◽

10.1111/j.1442-200x.1981.tb01243.x ◽

1981 ◽

Vol 23 (1) ◽

pp. 35-38 ◽

Cited By ~ 1

Author(s):

Ichiro Matsuda ◽

Izumi Akaboshi ◽

Jiro Yamamoto ◽

Noriyuki Nagata

Keyword(s):

Cell Lines ◽

Lymphoid Cell ◽

Biochemical Genetics ◽

Human Lymphoid Cell ◽

Lymphoid Cell Lines

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SPONTANEOUS PRODUCTION OF LEUCOCYTE MIGRATION INHIBITORY FACTOR (LIF) BY ESTABLISHED HUMAN LYMPHOID CELL LINES

Human Lymphokines ◽

10.1016/b978-0-12-406080-7.50025-4 ◽

1982 ◽

pp. 219-227

Author(s):

Ralph Ashorn ◽

Kai Krohn ◽

Kenneth Nilsson

Keyword(s):

Cell Lines ◽

Migration Inhibitory Factor ◽

Lymphoid Cell ◽

Inhibitory Factor ◽

Spontaneous Production ◽

Leucocyte Migration ◽

Human Lymphoid Cell ◽

Lymphoid Cell Lines

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Adhesion of human lymphoid cell lines to immobilized carbohydrates and to bone-marrow stromal cell layers by surface sugar receptors

International Journal of Cancer ◽

10.1002/ijc.2910540626 ◽

1993 ◽

Vol 54 (6) ◽

pp. 1017-1021 ◽

Cited By ~ 7

Author(s):

Sigrun Gabius ◽

Ralf Wawotzny ◽

Sabine Wilholm ◽

Ulrikc Martin ◽

Bernhard Wörmann ◽

...

Keyword(s):

Bone Marrow ◽

Cell Lines ◽

Lymphoid Cell ◽

Stromal Cell ◽

Bone Marrow Stromal Cell ◽

Marrow Stromal Cell ◽

Human Lymphoid Cell ◽

Cell Layers ◽

Sugar Receptors ◽

Lymphoid Cell Lines

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Arene–Ru(II)–chloroquine complexes interact with DNA, induce apoptosis on human lymphoid cell lines and display low toxicity to normal mammalian cells

Journal of Inorganic Biochemistry ◽

10.1016/j.jinorgbio.2010.05.002 ◽

2010 ◽

Vol 104 (9) ◽

pp. 967-977 ◽

Cited By ~ 40

Author(s):

Alberto Martínez ◽

Chandima S.K. Rajapakse ◽

Roberto A. Sánchez-Delgado ◽

Armando Varela-Ramirez ◽

Carolina Lema ◽

...

Keyword(s):

Cell Lines ◽

Lymphoid Cell ◽

Mammalian Cells ◽

Human Lymphoid Cell ◽

Low Toxicity ◽

Lymphoid Cell Lines

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The effects of cyclosporins on the cell cycle of T-lymphoid cell lines

Experimental Cell Research ◽

10.1016/0014-4827(82)90111-2 ◽

1982 ◽

Vol 140 (2) ◽

pp. 237-250 ◽

Cited By ~ 27

Author(s):

M KOPONEN ◽

A GRIEDER ◽

F LOOR

Keyword(s):

Cell Cycle ◽

Cell Lines ◽

Lymphoid Cell ◽

Lymphoid Cell Lines

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Cytotoxicity of farnesyltransferase inhibitors in lymphoid cells mediated by MAPK pathway inhibition and Bim up-regulation

Blood ◽

10.1182/blood-2011-02-334870 ◽

2011 ◽

Vol 118 (18) ◽

pp. 4872-4881 ◽

Cited By ~ 24

Author(s):

Husheng Ding ◽

Jennifer Hackbarth ◽

Paula A. Schneider ◽

Kevin L. Peterson ◽

X. Wei Meng ◽

...

Keyword(s):

Cell Lines ◽

Lymphoid Cell ◽

Mapk Pathway ◽

Lymphoid Cells ◽

Farnesyltransferase Inhibitors ◽

Death Domain ◽

Nucleotide Exchange ◽

Human Lymphoid Cell ◽

Induced Apoptosis ◽

Lymphoid Cell Lines

Abstract The mechanism of cytotoxicity of farnesyltransferase inhibitors is incompletely understood and seems to vary depending on the cell type. To identify potential determinants of sensitivity or resistance for study in the accompanying clinical trial (Witzig et al, page 4882), we examined the mechanism of cytotoxicity of tipifarnib in human lymphoid cell lines. Based on initial experiments showing that Jurkat variants lacking Fas-associated death domain or procaspase-8 undergo tipifarnib-induced apoptosis, whereas cells lacking caspase-9 or overexpressing Bcl-2 do not, we examined changes in Bcl-2 family members. Tipifarnib caused dose-dependent up-regulation of Bim in lymphoid cell lines (Jurkat, Molt3, H9, DoHH2, and RL) that undergo tipifarnib-induced apoptosis but not in lines (SKW6.4 and Hs445) that resist tipifarnib-induced apoptosis. Further analysis demonstrated that increased Bim levels reflect inhibition of signaling from c-Raf to MEK1/2 and ERK1/2. Additional experiments showed that down-regulation of the Ras guanine nucleotide exchange factor RasGRP1 diminished tipifarnib sensitivity, suggesting that H-Ras or N-Ras is a critical farnesylation target upstream of c-Raf in lymphoid cells. These results not only trace a pathway through c-Raf to Bim that contributes to tipifarnib cytotoxicity in human lymphoid cells but also identify potential determinants of sensitivity to this agent.

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