Knockdown of eukaryotic translation initiation factor 3 subunit B inhibits cell proliferation and migration and promotes apoptosis by downregulating WNT signaling pathway in acute myeloid leukemia.

The study aimed to investigate the effect of eukaryotic translation initiation factor 3 subunit B (EIF3B) on cell proliferation, migration, and apoptosis as well as the underlying mechanism in acute myeloid leukemia (AML). EIF3B expression was detected in AML-193, HL-60, OCI-AML2, and KG-1 cell lines and human primary bone marrow mononuclear cells (BMMC). EIF3B knockdown was realized by transfecting EIF3B ShRNA plasmids, and EIF3B knockdown and WNT2 overexpression were established by transfecting EIF3B ShRNA plasmids and WNT2 overexpression plasmids into KG-1 cells. The effect of EIF3B knockdown, and EIF3B knockdown plus WNT2 overexpression on cell proliferation, apoptosis, migration, glycogen synthase kinase 3B (GSK3B) and catenin beta 1 (CTNNB1) was assessed. EIF3B mRNA and protein expression were higher in AML-193, OCL-AML2 and KG-1 cell lines, but unchanged in the HL-60 cell line compared with human primary BMMC. The expression of WNT2 was decreased by EIF3B downregulation, while it had no effect on EIF3B expression. As for cell activities, EIF3B knockdown inhibited the cell proliferation and migration but promoted apoptosis by inhibiting WNT2 expression. In addition, EIF3B knockdown downregulated the expression of CTNNB1 but upregulated the expression of GSK3B by blocking WNT2 expression in AML, implying an inhibitory effect of EIF3B downregulation on WNT signaling pathway. EIF3B is upregulated and its knockdown inhibits cell proliferation, and migration, while promoting apoptosis by downregulating the WNT signaling pathway in AML.