Fig 2: Modulation of LIN7A expression abolished miR-501-3p-mediated functions in vivo.a Macrograph of tumors in all groups. b H&E-stained images of metastatic nodules in the lungs from all groups with magnification of the selected areas. Scale bar: 100 µm. Data depicts the mean ± standard deviation and are representative of three independent experiments

Fig 3: Modulation of LIN7A expression abolished miR-501-3p-mediated cellular activities in vitro.a Western blot showed the expression of LIN7A protein in HCCLM3-miR-501-3p cells that were transfected with LIN7A vector or PLC/PRF/5-anti-miR-501-3p cells that were transfected with shLIN7A vector and their corresponding controls. **P < 0.01. b Proliferation of HCCLM3-miR-501-3p that were transfected with LIN7A and PLC/PRF/5-anti-miR-501-3p cells that were transfected with shLIN7A vector and their corresponding controls was determined by CCK-8 assay. **P < 0.01. c Wound-healing assay and d transwell assay were performed to determine the effects of LIN7A on the migration and invasion of HCC cells. Scale bar: 100 µm, **P < 0.01. e LIN7A restoration decreased the expression of E-cadherin and increased the levels of N-cadherin, Vimentin, and Snail in miR-501-3p-overexpressing HCCLM3 cells. LIN7A knockdown abolished the effects of miR-501-3p loss on EMT process of PLC/PRF/5 cells. **P < 0.01. Data depicts the mean ± standard deviation and are representative of three independent experiments

Fig 4: a Absolute methylation levels of LIN7A, BASP1, EMB, and CEBPA in t(8;21) AML patients were higher than those in non-t(8;21) AML patients. b Absolute methylation levels of LIN7A, BASP1, EMB and CEBPA in de novo samples were higher than those in CR samples. c Distribution of CpG islands in the promoter region of the four genes. d Expression of LIN7A was much lower in patients with the t(8;21) translocation compared with that in other karyotypes according to TCGA dataset. e The expression levels of LIN7A positively correlated with the overall survival rate of AML patients. f LIN7A, BASP1, and EMB were identified as methylated genes in t(8;21) AML patients according to the GSE18700 dataset. g The methylation levels of LIN7A-probe 3 targeted sequence were significantly higher in patients with t(8;21) AML. h–i The methylation levels of the LIN7A-probe 3 targeted sequence negatively correlated with the h overall and i event-free survival rates of patients with t(8;21) AML. j Quantitative real-time polymerase chain reaction and k western blotting analyses showed increased mRNA and protein levels of LIN7A after treatment with 10 nM DAC for three (DAC-T3) or seven (DAC-T7) consecutive days. l Methylation-specific PCR of Kasumi-1 cells showed methylation of the probe 3-targeted sequence by two different paired primers. m LIN7A expression analysis determined by qRT-PCR after treatment with shLIN7A lentiviruses accompanied with or without 10 nM DAC in Kasumi-1 and SKNO-1 cells. n Western blot analysis of LIN7A expression change after treatment with shLIN7A lentiviruses accompanied with or without 10 nM DAC in Kasumi-1 and SKNO-1 cells. DMR Differentially methylated region; DAC Decitabine. *p < 0.05, **p < 0.01, and ***p < 0.001

Fig 5: Effect of LIN7A on cell apoptosis undertreatment with DAC in t(8;21) AML cell lines. a–d Effects of LIN7A on a, b Kasumi-1 and c, d SKNO-1 cell apoptosis. Cells were transfected with shRNA lentiviruses and treated with 10 nM DAC and 100 nM Ara-C. Cell apoptosis was assayed using Annexin V-FITC/propidium iodide double staining