Mounting evidence has shown that side population (SP) cells are enriched for cancer stem cells (CSCs) responsible for cancer malignancy. In this study, SP technology was used to isolate a small subpopulation of SP cells in human gallbladder cancer cell line GBC-SD, and SP cells which had superior potential for proliferation in vitro and tumorigenesis in vivo were identified. Importantly, the abundance of GBC-SD SP cells was increased by a transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT), and this effect was accompanied with a strong up-regulation of ABCG2 mRNA expression, and a decreased sensitivity to mitoxantrone. SP cells were restored upon the removal of TGF-β and the reversion of the cells to an epithelial phenotype, and smad3-specific siRNA reduced SP abundance in response to TGF-β. In conclusion, TGF-β-induced EMT by smad-dependent signaling pathway promotes cancer development and anti-cancer drug resistant phenotype by augmenting the abundance of GBC-SD SP cells, and a better understanding of mechanisms involved in TGF-β-induced EMT may provide a novel strategy for preventing cancer progression.

Mounting evidence has shown that side population (SP) cells are enriched for cancer stem cells (CSCs) responsible for cancer malignancy.In this study,SP technology was used to isolate a small subpopulation of SP cells in human gallbladder cancer cell line GBC-SD,and SP cells which had superior potential for proliferation in vitro and tumorigenesis in vivo were identified.Importantly,the abundance of GBC-SD SP cells was increased by a transforming growth factor-β (TGF-β)-induced epithelial-mesenchymal transition (EMT),and this effect was accompanied with a strong up-regulation of ABCG2 mRNA expression,and a decreased sensitivity to mitoxantrone.SP cells were restored upon the removal of TGF-β and the reversion of the cells to an epithelial phenotype,and smad3-specific siRNA reduced SP abundance in response to TGF-β.In conclusion,TGF-β-induced EMT by smad-dependent signaling pathway promotes cancer development and anti-cancer drug resistant phenotype by augmenting the abundance of GBC-SD SP cells,and a better understanding of mechanisms involved in TGF-β-induced EMT may provide a novel strategy for preventing cancer progression.

【Objective】 To report the antibody specific identification process of a pregnant woman who had no history of blood transfusion but presented high-frequency anti-Jr^a antibodies. 【Methods】 Antibody screening and identification were performed by saline and indirect Coomb’s technique (microcolumn gel card, PEG). ABO, Rh and other blood group antigens were identified by saline. Further antibody identification tests were performed by the reaction between cells treated with various enzymes and patient plasma. Jr^a antigen was identified by human anti-Jr^a antibody. JR blood type genotyping was performed by MALDI-TOF mass spectrometry detection system. Antibody titer in serum was tested. 【Results】 The patient′s blood type was O with RhD(+ ) and CcDEe. The plasma reacted negatively with antibody screening and identification cells by saline, but positively by indirect globulin test. The self-control was negative. The patient′s Jr^a antigen was negative in serological tests and mass spectrometry blood type genotyping. Mass spectrometry revealed a homozygous nonsense mutation (c.376C>T) in exon 4. The anti-Jr^a antibody titer was 1∶2. 【Conclusion】 The patient developed high-frequency anti-Jr^a antibodies during pregnancy.