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.