We examined the regulation of apoptosis by COX-2 in a human CRC cell line. HCA7 cells have previously been reported to express high levels of COX-2 with abundant PGE 2 generation (Sheng et al, 1997) . Apoptosis was quantified by fluorescence labelling with FITC-conjugated antibody to Annexin V and propidium iodide assessed by flow cytometry (Figure 1 ). Following a 24 h treatment with the selective COX-2 inhibitor SC236 (5 mM), a significant decrease (P ¼ 0.01) in HCA7 cells viability was observed ( Figure 1B ), mirrored by a doubling of the proportion of the cell population gated to the early apoptosis phase (Annexin V positive, propidium iodide negative) ( Figure 1B ). The observed increase in apoptosis at low micromolar doses of SC236 was prevented by coadministration of exogenous PGE 2 (1 mM), whereas more marked increases in apoptosis seen with higher doses of SC236 were not rescued. A similar effect was noted with regard to effects on cell proliferation (see Supplementary Figure S1 ). The ability of PGE 2 to promote cell survival confirmed that at low micromolar doses the effects of SC236 are largely dependant on its ability to inhibit COX-2.