Metabolism of alkyl lysophospholipid in epithelial cancer cell lines and inhibition of cell growth

1993 ◽  
Vol 71 (3-4) ◽  
pp. 122-126 ◽  
Author(s):  
Xiaoli Lu ◽  
Xi Zhou ◽  
Dawn Kardash ◽  
Gilbert Arthur
Keyword(s):  
Cell Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
A549 Cell ◽  
Inhibitory Effects ◽  
Epithelial Cancer ◽  
Cancer Cell Growth ◽  
Mechanism Of Inhibition ◽  
Growth Inhibitory ◽  
Inhibit Cell Growth

The mechanism of inhibition of cancer cell growth by alkyllysophospholipids is not known. We have investigated the metabolism of 1-O-octadecyl-2-O-methylglycerophosphocholine (ET-18-OCH3) in MCF7, A427, and A549 cell lines to determine whether there is a correlation between metabolism and sensitivity and whether the growth-inhibitory effects are due to ET-18-OCH3 or its metabolites. After 12 h incubation with ET-18-OCH3, less than 1.5% of ET-18-OCH3 taken up in the cells was converted to 1-O-octadecyl-2-O-methylglycerol (OMG). No correlation was observed between the extent of metabolism and sensitivity to the compound. Incubation of cells with 1 μg OMG/mL (2.8 μM) for 12 h resulted in cellular quantities of OMG in MCF7, A427, and A549 that were, respectively, 8-, 5-, and 25-fold greater than those in cells incubated with 5 μg ET-18-OCH3/mL (9.6 μM). While 12 h incubation with 1 μg OMG/mL did not significantly inhibit the proliferation of MCF7 or A427 cells, incubation with 5 μg ET-18-OCH3/mL inhibited MCF7 and A427 growth by 90 and 15%, respectively. A549 cell growth was inhibited 10% by 1 μg OMG/mL, but not by 5 μg ET-18-OCH3/mL. Incubation of cells for 12 h with 5 μg OMG/mL (13.9 μM) inhibited the growth of all three cell lines. Our results indicate that both ET-18-OCH3 and OMG can inhibit cell growth but the low quantities of OMG produced from ET-18-OCH3 are not responsible for the observed inhibition of MCF7 and A427 cell growth.Key words: alkyllysophospholipid, metabolism, epithelial cancer cells, growth inhibition.

Enhancing the Cancer Cell Growth Inhibitory Effects of Table Grape Anthocyanins

2018 ◽  
Vol 83 (9) ◽  
pp. 2369-2374 ◽  
Author(s):  
Karnell L. Grimes ◽  
Connor M. Stuart ◽  
Justin J. McCarthy ◽  
Baljinder Kaur ◽  
Emilio J. Cantu ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Table Grape ◽  
Inhibitory Effects ◽  
Cancer Cell Growth ◽  
Growth Inhibitory

Screening for naturally occurring oxyprenylated secondary metabolites as cancer cell growth inhibitory agents

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
F Epifano ◽  
S Genovese ◽  
P Lullo ◽  
S Fiorito ◽  
G Trivisonno ◽  
...  
Keyword(s):  
Cell Growth ◽  
Secondary Metabolites ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Naturally Occurring ◽  
Growth Inhibitory ◽  
Inhibitory Agents

Synthesis of Analogs of 2-Methoxyestradiol with Enhanced Inhibitory Effects on Tubulin Polymerization and Cancer Cell Growth

1997 ◽  
Vol 40 (15) ◽  
pp. 2323-2334 ◽  
Author(s):  
Mark Cushman ◽  
Hu-Ming He ◽  
John A. Katzenellenbogen ◽  
Ravi K. Varma ◽  
Ernest Hamel ◽  
...  
Keyword(s):  
Cell Growth ◽  
Cancer Cell ◽  
Tubulin Polymerization ◽  
Inhibitory Effects ◽  
Cancer Cell Growth

Cyclin D1 antisense RNA destabilizes pRb and retards lung cancer cell growth

1997 ◽  
Vol 273 (5) ◽  
pp. L941-L949 ◽  
Author(s):  
Barbara Driscoll ◽  
Lingtao Wu ◽  
Susan Buckley ◽  
Frederick L. Hall ◽  
Kathryn D. Anderson ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cell Death ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Cell ◽  
Cyclin D ◽  
Lung Cancer Cell ◽  
Cancer Cell Growth ◽  
Transfected Cells ◽  
The Impact

To investigate the role of cyclin D1 in the regulation of lung cancer cell growth, we created five stably transfected cell lines carrying a cyclin D1 antisense construct. The transfected cells exhibited a marked decrease in the rate of cell growth, in contrast to the original lines (A549 and NCI-H441). The expression of several cell cycle-regulating proteins, including cyclin A, the cyclin-dependent kinases (cdk) 2 and cdk4, in addition to cyclin D1 itself, was markedly decreased. The expression of one cdk inhibitor, p21WAF1/CIP1, increased in the A549-derived cell lines. A specific target of cyclin D1 activity, the growth-suppressing product of the retinoblastoma gene, pRb, exhibited decreased expression and a decreased level of phosphorylation in the transfected cells. Decreased expression of pRb due to a significant increase in its turnover rate suggested that the stability of the protein may depend on phosphorylation by cyclin D1-dependent cdk activity. In addition to the impact on pRb stability, decreased expression of cyclin D1 induced susceptibility to cell death after withdrawal of exogenous growth factors in the antisense transfected cell lines, a response that was not observed in the original cancer cell lines. We conclude that abrogation of cyclin D1 overexpression in lung cancer cells disrupts several key pathways that are required for uncontrolled cell growth and induces those that lead to cell death after growth factor deprivation. Therefore, we speculate that use of antisense cyclin D1 expression in appropriate gene vectors could be a useful method for retarding lung cancer cell growth in accessible tumors such as those of the lung epithelium.

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