Objective To investigate the regulatory mechanism of bone marrow mesenchymal stem cells(BMSC) on the biological profiles of KATO-Ⅲcell lines of gastric cancer. Methods Transwell cubicle was applied to build the co-cultured model in non-contact style. The differences of cell proliferation and the resistance of anti-tumour drug (5-fluoropyrimidinedione, 5-FU and Cisplatin, CDDP) between co-cultured group and single cultured group were evaluated by Cell Counting Kit 8-assay (CCK-8). The invasion ability was detected by Transwell assay. The expressions of stem cell makers, apoptosis-related factors and epithelium-mesenchymal transition (EMT)-related factors were detected by RT-PCR. Results The proliferation ability of KATO-Ⅲ cells in co-cultured group was significantly stronger than that in single cultured group. The growth rate of KATO-Ⅲ cells in co-cultured group was significantly higher than that in single cultured group after treatment of 5-FU and CDDP (P<0.05). The mRNA expression level of Bcl-2 was significantly higher in co-cultured group KATO-Ⅲ cells (P<0.05), while the mRNA expression level of Bax was significantly lower in co-cultured group KATO-Ⅲ cells(P<0.05) in comparison with those in single cultured group. As compared to KATO-Ⅲ cells in single cultured group, the number of infiltrating-membrane cells was significantly higher (37.33±5.22 vs 14.56±2.54, P<0.01) in co-cultured group, and the mRNA expression levels of Snail and N-cadherin were significantly higher in co-cultured group KATO-Ⅲ cells (P<0.05), while the mRNA expression level of E-cadherin was significantly lower in co-cultured group KATO-Ⅲ cells (P<0.05). The expressions of CD133, Nanog and Sox-2 mRNA in co-cultured group KATO-Ⅲ cells were significantly higher than those in single cultured group (P<0.05). Conclusions In co-cultured model sharing non-contact style, BMSC can enhance such properties of KATO-Ⅲ gastric cancer cells as the proliferation, the invasion and the chemoresistance. Furthermore, the regulatory mechanisms may be related to the increase of the expressions of some stem cell markers in gastric cancer cells.

Objective To investigate the regulatory mechanism of bone marrow mesenchymal stem cells(BMSC) on the biological profiles of KATO-Ⅲcell lines of gastric cancer. Methods Transwell cubicle was applied to build the co-cultured model in non-contact style. The differences of cell proliferation and the resistance of anti-tumour drug (5-fluoropyrimidinedione, 5-FU and Cisplatin, CDDP) between co-cultured group and single cultured group were evaluated by Cell Counting Kit 8-assay (CCK-8). The invasion ability was detected by Transwell assay. The expressions of stem cell makers, apoptosis-related factors and epithelium-mesenchymal transition (EMT)-related factors were detected by RT-PCR. Results The proliferation ability of KATO-Ⅲ cells in co-cultured group was significantly stronger than that in single cultured group. The growth rate of KATO-Ⅲ cells in co-cultured group was significantly higher than that in single cultured group after treatment of 5-FU and CDDP (P<0.05). The mRNA expression level of Bcl-2 was significantly higher in co-cultured group KATO-Ⅲ cells (P<0.05), while the mRNA expression level of Bax was significantly lower in co-cultured group KATO-Ⅲ cells(P<0.05) in comparison with those in single cultured group. As compared to KATO-Ⅲ cells in single cultured group, the number of infiltrating-membrane cells was significantly higher (37.33±5.22 vs 14.56±2.54, P<0.01) in co-cultured group, and the mRNA expression levels of Snail and N-cadherin were significantly higher in co-cultured group KATO-Ⅲ cells (P<0.05), while the mRNA expression level of E-cadherin was significantly lower in co-cultured group KATO-Ⅲ cells (P<0.05). The expressions of CD133, Nanog and Sox-2 mRNA in co-cultured group KATO-Ⅲ cells were significantly higher than those in single cultured group (P<0.05). Conclusions In co-cultured model sharing non-contact style, BMSC can enhance such properties of KATO-Ⅲ gastric cancer cells as the proliferation, the invasion and the chemoresistance. Furthermore, the regulatory mechanisms may be related to the increase of the expressions of some stem cell markers in gastric cancer cells.