目的 探讨免疫球蛋白γ-1重链恒定区（immunoglobulin γ-1 heavy chain constant region，IGHG1）在急性髓系白血病（acute myeloid leukemia，AML）THP-1细胞中的表达以及调控转化生长因子β（transforming growth factor-β，TGF-β）/Smad通路对细胞增殖、凋亡和侵袭的影响。方法 以9例AML患儿的骨髓标本、8例骨折患儿的骨髓标本、人骨髓基质细胞HS-5及人AML细胞THP-1、HL60为研究对象，Western blot检测IGHG1蛋白表达；将THP-1细胞分组为空白（细胞未经任何处理）、si-NC、si-IGHG1-1、si-IGHG1-2、si-IGHG1-3、TGF-β、si-IGHG1-1 TGF-β、si-IGHG1-1 TGF-β LY364947（TGF-β/Smad通路抑制剂）组，CCK-8法检测细胞增殖；流式细胞术检测细胞凋亡；Transwell实验检测细胞侵袭，Western blot检测细胞中IGHG1、TGF-β、p-Smad2、p-Smad3蛋白表达。结果 与骨折患儿骨髓比较，AML患儿骨髓中IGHG1蛋白[（0.24?.03）vs（0.87?.12]表达水平显著升高（P＜0.05）；与HS-5细胞比较，THP-1、HL60细胞中IGHG1蛋白[(0.89?.14) (0.75?.08) vs (0.21?.02)]表达升高（P＜0.05）；与空白组比较，si-IGHG1-1组THP-1细胞OD450值（24、48、72 h），侵袭细胞数目，TGF-β、p-Smad2、p-Smad3蛋白表达均显著降低，细胞凋亡率升高，TGF-β组对应指标呈相反变化（P＜0.05）；TGF-β逆转了沉默IGHG1对THP-1细胞增殖、凋亡和侵袭的影响；与si-IGHG1-1 TGF-β组比较，si-IGHG1-1 TGF-β LY364947组TGF-β、p-Smad2、p-Smad3蛋白、OD450值（24、48、72 h）及侵袭细胞数目显著降低，细胞凋亡率升高（P＜0.05）结论 IGHG1在AML细胞中高表达，沉默IGHG1可抑制AML细胞增殖及侵袭，并促进AML细胞凋亡，该机制可能与抑制TGF-β/Smad通路有关。
Objective To investigate the expression of immunoglobulin γ-1 heavy chain constant region (IGHG1) in acute myeloid leukemia (AML) THP-1 cell and its influences on cell proliferation, apoptosis and invasion by regulating the transforming growth factor β (TGF-β)/Smad pathway. Methods The bone marrow specimens of 9 children with AML, the bone marrow specimens of 8 children with fracture,human bone marrow stromal cells HS-5 and human AML cells THP-1, HL60 were used as research objects,Western Blot was used to detect IGHG1 protein expression; THP-1 cells were divided into: blank group (cells without any treatment), si-NC group, si-IGHG1-1 group, si-IGHG1-2 group, si-IGHG1-3 group, TGF-β group,si-IGHG1-1 TGF-β group,si-IGHG1-1 TGF-β LY364947 group, CCK-8 method was used to detect cell proliferation; apoptosis was detected by flow cytometry; Transwell experiment was used to detect cell invasion ; Western blot was used to detect the protein expression of IGHG1, TGF-β, p-Smad2, and p-Smad3 in each group of cells. Results Compared with the bone marrow of children with fracture, the expression level of IGHG1 protein [(0.24?.03) vs (0.87?.12] in the bone marrow of children with AML was significantly higher (P<0.05); compared with HS-5 cell, the expression level of IGHG1 protein in human AML cells THP-1, HL60 was significantly increased [(0.89?.14)(0.75?.08) vs (0.21?.02)] (P<0.05); compared with the blank group , the OD450 value (24, 48, 72h) of THP-1 cells, the number of invaded cells, and the protein expression of TGF-β, p-Smad2, and p-Smad3 were significantly reduced in the si-IGHG1-1 group, and the apoptosis rate was increased (P<0.05), while the corresponding indexes in TGF-β group were opposite (P<0.05); the TGF-β reversed the effects of silencing IGHG1 on the proliferation, apoptosis and invasion of THP-1 cells; compared with si-IGHG1-1 TGF-β group, TGF-β, p-Smad2, p-Smad3 protein, OD450 values (24, 48, 72 h) and invasion number of cells decreased significantly in si-IGHG1-1 TGF-β LY364947 group, and the cell apoptosis rate was increased (P<0.05). Conclusions IGHG1 is highly expressed in AML cells. Silencing IGHG1 can inhibit the proliferation and invasion of AML cells, and promote the apoptosis of AML cells. This mechanism may be related to the inhibition of TGF-β/Smad pathway.