Figure 1.

IKKβ/TSC1/mTOR pathway was activated in Barrett’s esophagus–associated EAC cancer cells. A, increased expression of pIKKβ (S¹⁸¹) was correlated with higher level of pTSC1 (S⁵¹¹) and pS6K1 (T³⁸⁹) in SEG-1 and BE3 EAC cancer cell lines. Immortalized Barrett’s esophagus cell lines CPC-A and CPC-C had lower expression level of pIKKβ (S¹⁸¹) and expressed concurrently low levels of pTSC1 (S⁵¹¹) and pS6K1 (T³⁸⁹). The SKGT4 EAC cancer cell line also had lower expression of pIKKβ (S¹⁸¹), pTSC1 (S⁵¹¹), and pS6K1 (T³⁸⁹). B, the phosphorylation of pTSC1 (S⁵¹¹) and pS6K1 (T³⁸⁹) increased two to three times in SEG-1 cancer cells treated with 300 μmol/L CDCA (P < 0.001) and low-pH medium (P < 0.001) compared with those in untreated cells. C, conjugated bile acid TCDA increased the expressions of pTSC1 (S⁵¹¹) and pS6K1 (T³⁸⁹), and the IKKβ inhibitor Bay 11-7082 blocked the TCDA stimulation effect in SEG-1 EAC cancer cells. D, cell proliferation was increased in SEG-1 and BE3 cancer cells compared with SKGT-4 cells, which had lower expression of the IKKβ/TSC1/mTOR signaling pathway.