Table 1.

Formation of PGEs in cellular COX peroxidation and cell growth response. Cell cycle analysis (PI staining) and cell proliferation assays (MTS) of HCA-7 colony 29 cells treated with AA, DGLA and DGLA in combination with CP-24879.

Cells (HCA-7 Colony 29) Cultured w/	Formation of PGs (nM/2×106 cells)						Cell Cycle Distribution			Cell Proliferation
	[PGE1]			[PGE2]			% in G1 Phase			% Viability
	8 h	24 h	48 h	8 h	24 h	48 h	8 h	24 h	48 h	48 h
Controla		N.D.b		0.9±0.2	0.6±0.4	N.D.	36.6±1.6	40.3±3.8	44.6±2.2	100
AA (100 µM)		N.D.		101.5±5.3	80.6±6.0	68.6±7.9	40.4±7.2	41.6±3.8	43.7±3.2	112.1±3.9
DGLA (100 µM)	81.3±0.3	70.6±2.2	48.1±1.9	19.3±0.3	32.6±1.7	48.6±0.5	46.3c±7.6	42.7±2.3	38.3±1.2	109.1±5.7
DGLA w/ 5.0 µM CP	92.3±4.2	76.8±8.3	64.0±6.3	6.8±1.3	9.3±3.9	14.4±5.4	44.5c±5.2	47.0c±3.4	45.3±2.6	98.3d±5.0

^a% cell viability was compared with control group. Control cells were incubated with 0.1 % dimethylsulfoxide and 0.1 % ethanol (final concentration);

^bno detected or data represent the mean ± SD derived from three separate experiments with triplicate wells per condition;

^cP < 0.05, significant G₁ delay vs. corresponding controls; and

^dsignificantly different vs. treatment of AA and DGLA. In addition, G₂/M phase delays were also observed from 8 h treatments of DGLA and 8 h-24 h treatment of DGLA with CP24879 (data not shown).