Aim: To investigate the role of c-Jun N-terminal kinase (JNK) in thermotherapy-induced apoptosis in human gastric cancer SGC-7901 cells.Methods: Human gastric cancer SGC-7901 cells were resuscitated and cultured in vitro.SGC-7901 cells with thermotherapy treatment at 43oC for 0, 0.5, 1, 2 and 3h were cultured 24 h.Apoptosis was evaluated by TUNEL immunostaining and Annexin vs PI flow cytometry, while cell proliferation was observed by MTT.p-JNK, Bcl-2, Bax and caspase-3 proteins production was evaluated by Western blot.The expression of JNK at mRNA level was determined by RT-PCR.Results: The growth of gastric carcinoma SGC7901 cells was inhibited significantly after thermotherapy treatment by MTT, which was 32.7%, 30.6%, 43.8%,52.9% at 0.5, 1,2, and 3h post thermotherapy, respectively.Flow cytometry analysis revealed that the G0/G 1 phase of SGC7901 cells treated with thermotherapy at 1 and 2 h was increased, but S phase reduced (P<0.05), compared to that of SGC7901 cells untreated with thermotherapy.This is consistent with significantly increased apoptotic rate of SGC7901 cells treated with thermotherapy for 0.5 h, 1 h, 2 h and 3 h, compared with that of SGC7901 cells untreated group (46.5% ± 0.23%, 39.9% ± 0.53%, 56.6% ± 0.35%, and 50.4% ± 0.29% vs 7.3% ± 0.10%, P< 0.01),respectively.This is supported by the TUNEL assay (48.2% ± 0.4%, 40.1% ± 0.2%, 61.2% ± 0.29%, and 52.0%± 0.42% vs 12.2% ± 0.22%, P< 0.01).More importantly, the expression of p-JNK protein and JNK mRNA levels were significantly higher at 0.5 h than that of 0 h post treatment (P<0.01), and reached its maximal peak at 2 h.Similar pattern was seen in Bax and Caspase-3 proteins induced by thermotherapy.While Bcl-2 was increased at 0.5 h, to the peak at 1 h, and followed by a decrease after 1 h.Furthermore, JNK specific inhibitor (SP600125)suppresses p-JNK, Bax and caspase-3 at protein level in the cells with thermotherapy, compared to mock-inhibitor treatment, which is in line with decrease of apoptotic rate.While the expression of Bcl-2 was consistent with thermotherapy alone.Conclusion: Thermotherapy induces apoptosis in gastric cancer cells via promoting phosphoJNK at message and protein levels, and up-regulating the expression of Bax, caspase-3 proteins, while Bcl-2,maybe plays an protective role in this process.Therefore, activation of JNK via Bax-Caspase-3 pathway may be important in thermotherapy inducing apoptosis in gastric cancer cells.