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Objective To investigate the effects of metformin combined with gemcitabine on the proliferation，migra⁃ tion，and epithelial-mesenchymal transition（EMT）of pancreatic cancer cells. Methods The pancreatic cancer PANC-1 cells were selected and subcultured. The cell proliferation activity was measured by MTT assay when the final metformin concentrations were 0，5，10，20，40 mmol/L or the final gemcitabine concentrations were 0，0. 1，0. 2，0. 4，0. 8 μmol/L， and the follow-up experiments were carried out with the concentrations of metformin and gemcitabine that could reduce the cell proliferation activity to about 50%. Besides，PANC-1 cells were selected again and were randomly divided into three groups：the control group，metformin group，gemcitabine group，and combination group. The cells were treated with met⁃ formin or/and gemcitabine. The cell migration rate was measured by cell scratch assay. The expression levels of E-cad⁃ herin and Vimentin was detected by Western blotting. Results The proliferation activity of PANC-1 cells decreased with the increased concentrations of metformin and gemcitabine，in a concentration-dependent manner（F= 29. 14，66. 88， both P<0. 01）. After giving metformin（20 mmol/L）and gemcitabine（0. 4 μmol/L），the proliferation activity of PANC-1 cells decreased to about 50%，so the follow-up experiments were conducted with these concentrations. The cell migration rates and the expression levels of E-cadherin and Vimentin in the metformin group，gemcitabine group，and combination group were lower than those in the control group；the cell migration rate and the expression levels of E-cadherin and Vimen⁃ tin in the combination group were lower than those in the metformin and gemcitabine groups（all P<0. 05）. There was no significant difference in the cell migration rate or expression levels of E-cadherin and Vimentin between the metformin group and gemcitabine group（all P>0. 05）. Conclusion The combination therapy of metformin and gemcitabine can inhibit the proliferation，migration and EMT of pancreatic cancer cells，and metformin improves the chemosensitivity of pancreatic cancer cells to gemcitabine. [ABSTRACT FROM AUTHOR]

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目的探讨生长抑素(SST)对人肝癌细胞系Hep G2上皮间质转化(EMT)的影响及其可能机制。方法取对数生长期Hep G2细胞,随机分为对照组及SST低、中、高剂量组,分别给予0、100、200、400μg/m L SST处理。各组继续培养24 h,采用MTT法检测细胞增殖能力(细胞存活率),Transwell小室法检测细胞迁移能力(跨膜细胞数),Western blotting法检测细胞E-钙黏蛋白(E-cadherin)和波形蛋白(Vimentin)表达。结果对照组及SST低、中、高剂量组细胞存活率依次为100%、(78.7±6.36)%、(68.0±6.66)%和(44.0±7.23)%,跨膜细胞数依次为(53±6)、(41±2)、(28±5)和(22±3)个。SST低、中、高剂量组细胞存活率、跨膜细胞数均低于对照组(P均<0.05),且随着SST浓度升高,细胞存活率、跨膜细胞数逐渐降低(F分别为79.13、51.71,P均<0.05)。对照组及SST低、中、高剂量组E-cadherin相对表达量依次为0.20±0.04、0.28±0.04、0.46±0.06和0.75±0.07,Vimentin相对表达量依次为1.17±0.15、0.79±0.04、0.54±0.08和0.57±0.06;SST低、中、高剂量组E-cadherin相对表达量均高于对照组、Vimentin相对表达量均低于对照组(P均<0.05),且随着SST浓度升高,E-cadherin相对表达量逐渐升高(P均<0.05),而Vimentin相对表达量降低(P均<0.05)。结论 SST可抑制人肝癌细胞系Hep G2的侵袭能力,其机制可能与增加E-cadherin蛋白表达、降低Vimentin蛋白表达,继而逆转Hep G2细胞的EMT有关。 [ABSTRACT FROM AUTHOR]