We used immunochemistry to demonstrate expression of acetylcholine's nicotinic α7-receptor subtype in human colon cancer cell line HT-29. Moreover, RT-PCR and immunochemistry showed that choline acetyltransferase and acetylcholine esterase, the enzymes responsible for acetylcholine synthesis and degradation, respectively, localise in HT-29 cells. Bromoacetylcholine bromide, an inhibitor of choline acetyltransferase, significantly attenuated basal cell growth. Our findings suggest that acetylcholine might serve as an autocrine/paracrine–or speculatively, even intracrine–signalling molecule in cell line HT-29, thus contributing to carcinogenesis/cancer progression.