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Role for ceramide in cell cycle arrest

S Jayadev¹, B Liu, A E Bielawska

¹Department of Cell Biology, Duke University Medical Center, Durham, North Carolina 27710.

The Journal of Biological Chemistry

|February 3, 1995

Summary

Serum withdrawal halts leukemia cell cycle progression and induces apoptosis by increasing ceramide levels. Diacylglycerol counteracts ceramide

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Area of Science:

Cell Biology
Molecular Biology
Biochemistry

Background:

Cellular dependence on serum factors for growth suggests antimitogenic pathways.
Ceramide is investigated as a potential intracellular mediator of this serum factor dependence.

Purpose of the Study:

To investigate ceramide's role in serum factor-dependent cell cycle arrest and apoptosis.
To explore the involvement of the diacylglycerol/protein kinase C pathway in modulating these responses.

Main Methods:

Molt-4 leukemia cells were subjected to serum withdrawal.
Changes in cell cycle progression, apoptosis, ceramide, and diacylglycerol levels were measured.
Exogenous ceramide and diacylglycerol were added to assess their effects.

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Main Results:

Serum withdrawal induced G0/G1 cell cycle arrest and apoptosis.
This was accompanied by increased sphingomyelin hydrolysis and ceramide levels.
Exogenous ceramide mimicked cell cycle arrest but enhanced apoptosis.
Diacylglycerol attenuated ceramide-induced apoptosis but not cell cycle arrest.

Conclusions:

Ceramide plays a novel role in regulating cell cycle progression.
A lipid signaling pathway involving ceramide and diacylglycerol mediates serum withdrawal effects.
This study provides evidence for an intracellular signal transduction pathway controlling cell cycle arrest.