Tumor growth of colorectal cancers accompanies up-regulation of inducible cyclooxygenase-2, which catalyzes a key step in conversion of arachidonic acid to prostaglandin H₂ (PGH₂) (Marx, 2001). In the downstream of COX, thromboxane synthase (TXS) catalyzes the conversion of PGH₂ to thromboxane A₂ (TXA₂). We found recently that TXS is significantly up-regulated in the human colorectal carcinomas (Sakai et al. 2003). TXS was also highly expressed in human colonic cancer cell lines. Disruption of TXS protein by the antisense oligonucleotide inhibited the proliferation of the cancer cells (Suzuki et al. 2004). Herein we investigated if the K_v7.1 (K_vLQT1), a voltage-dependent K⁺ channel, is involved in the TXA₂-induced cell proliferation. Human colorectal cancer tissue and its accompanying normal mucosa were obtained from surgical resection of Japanese patients in accordance with the recommendations of the Declaration of Helsinki and with the ethics committee approval. The expression of K_v7.1 protein in human tissues and human colonic carcinoma cell lines was examined by Western blotting. Cell proliferation assay was performed by counting the number of the cell in a 12-well plate. Results are shown as means ± S.E.M. The data were statistically analysed using one-way ANOVA and Tukey’s multiple comparison test. We compared the expression levels of K_v7.1 protein between human colorectal cancer tissue and its accompanying normal mucosa. It was found that K_v7.1 is up-regulated in human cancer tissues (70 kDa; 10 of 10 cases, 100%). Significant expression of K_v7.1 protein was also observed in the human colonic cancer cell lines such as KM12-L4, HT-29, T-84, WiDr (n = 3). A stable analog of TXA₂ (STA₂; 0.1 μM) stimulated the proliferation of KM12-L4 cells from (1.31 ± 0.03) x 10⁵ to (1.65 ± 0.04) x 10⁵ cells (n = 5, P < 0.01), and the STA₂-induced effect was completely inhibited by chromanol 293B (10 μM), an inhibitor of K_v7.1 (n = 5, P < 0.01). STA₂ (0.1 μM) significantly increased the expression level of K_v7.1 protein by (2.09 ± 0.09)-fold in the KM12-L4 cells (n = 4, P < 0.01). In the cells, STA₂ also increased the chromanol 293B-sensitive K⁺ current from 8.87 ± 1.01 to 16.91 ± 1.25 pA pF^-1 at +30 mV (n = 7, P < 0.01). These results suggest that paralleled up-regulations of TXS and K_v7.1 channel may be involved in the tumor growth of human colorectum.