Objective:To investigate the expression of herg1 gene in tumor tissues from gastric carcinomas and gastric carcinoma cell lines,and study the relationship between HERG K+ channel expressions and tumor cell proliferation and apoptosis. Methods:RT-PCR and PCR assays were used to detect the expression of herg1 gene in 64 gastric carcinomas and the gastric cancer cell line SGC-7901. Blocking the HERG K+ channels was used to evaluate their effects on tumor cell proliferation and apoptosis. Results:The statistically significant expression of herg1 gene was detected in all the gastric cancers and SGC-7901 cells,but not in normal tissues. The HERG K+ channel blocker,E-4031,increased the cell population in G0/G1(P < 0.05) and the number of apoptotic tumor cells(P < 0.05). Conclusion:HERG K+ channels were expressed in all gastric carcinomas tested and these channels appear to modulate tumor cell proliferation and apoptosis.
Objective:To investigate the effect of Rapamycin on epithelial-mesenchymal transition(EMT) of LoVo colonic adenocarcinoma cells in vitro. Methods:Cultured LoVo colonic adenocarcinoma cells were divided into three groups: negative control group,EMT-inducing group(TGF-β1) and EMT-interfering group(TGF-β1 plus Rapamycin). E-cadherin expression in LoVo cells was detected by Western Blot,while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT-PCR. Results:TGF-β1 induced LoVo cell switching from polygonal to spindle-shaped. TGF-β1 enhanced the expression of vimentin,but lowered the level of E-cadherin. In contrast,Rapamycin impaired the transition induced by TGF-β1. Rapamycin dramatically abrogated TGF-β1-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the up-regulation of Snail mRNA expression induced by TGF-β1. Conclusion:Rapamycin dramatically abrogated TGF-β1 induced Snail mRNA expression in LoVo cells,hence inhibiting EMT of these cells in vitro.
Renhu Sun Jiang Li Jing Cui Qing Lv Xinghua Liu Guobin Wang