Fig 1: MBP1 is regulated by HIF-1a under hypoxic conditions. (A) MDA231 and (B) MCF7 cells were cultured under hypoxic conditions (1% O2) for 24 h, then the protein expression levels of HIF-1a, MBP1 and ß-catenin were analyzed using western blot analysis. (C) MDA231 and (D) MCF7 cells were cultured in CoCl2 for 24 h, then the protein expression levels of HIF-1a, MBP1 and ß-catenin were detected using western blot analysis. (E) MDA231 and (F) MCF7 cells were cultured under hypoxic conditions (1% O2) or CoCl2 for 24 h, then the mRNA expression levels of MBP1 and ß-catenin were detected using reverse transcription-quantitative PCR. Whole cell lysates of the MDA231 cell line were immunoprecipitated with (G) anti-MBP1 or IgG, or (H) anti-HIF-1a or IgG, then subjected to western blot analysis for MBP1 and HIF-1a. All the data are presented as the mean ± SD from three independent experiments. **P<0.01. MBP-1, c-Myc promoter binding protein 1; HIF-1a, hypoxia-inducible factor 1a; n.s., not significant.
Fig 2: MiR-942-3p had a negative correlation with mannose-binding lectin 2 (MBL2) expression in patients with hepatocellular carcinoma (HCC). A, The Cancer Genome Atlas (TCGA) analysis of the expression levels of 14 target genes of miR-942-3p in paired HCC tissues (n = 23). B and C, Pearson correlation analysis revealed that miR-942-3p had a negative correlation with MBL2 expression rather than other target genes in HCC tissues. D, Receiver operating characteristic (ROC) curve was used to determine a cutoff value of MBL2 in patients with HCC. E, Patients with HCC were divided into high or low MBL2 expression group according to the cutoff value. F, Kaplan-Meier analysis demonstrated that the patients with high MBL2 expression displayed a better survival but had no difference in tumor recurrence as compared with those with low MBL2 expression in patients with HCC.
Fig 3: MBP1 inhibits BC growth in vivo. (A) Representative images of xenografts in the Lv-MBP1 and Lv-NC groups 21 days following inoculation. The expression level of MBP1 from the tumors was analyzed using (B) western blot analysis, (C) reverse transcription-quantitative PCR and (D) immunohistochemistry between the LV-MBP1 and LV-NC groups. Scale bar, 50 µm. Tumor (E) volume and (F) weight in the LV-MBP1 and LV-NC groups. All the data are presented as the mean ± SD. *P<0.05 and **P<0.01. MBP1, c-Myc promoter binding protein 1; NC, negative control; Lv-MBP1, MBP1 overexpression vector.
Fig 4: Identification of mannose-binding lectin 2 (MBL2) as a direct target of miR-942-3p in hepatocellular carcinoma (HCC) cells. A and B, Quantitative polymerase chain reaction (qPCR) and Western blot analysis of the effects of miR-942-3p mimic or inhibitor on the messenger RNA (mRNA) and protein levels of MBL2 in LO2 or HepG2 cell line. C, The binding sites of miR-942-3p with wild-type (WT) or mutant (Mut) 3'-untranslated region (3'-UTR) of MBL2. D, The luciferase activities of WT or Mut 3'-UTR of MBL2 after cotransfection with miR-942-3p mimic or inhibitor and WT or Mut 3'-UTR of MBL2 in HCC cells. Data were given as mean ± standard error of the mean of 3 experiments. *P< .05.
Fig 5: Mannose-binding lectin 2 (MBL2) reversed the tumor-promoting effects of miR-942-3p in hepatocellular carcinoma (HCC) cells. A, Quantitative polymerase chain reaction (qPCR) and Western blot analysis of the transfection efficiency of MBL2 plasmid or si-MBL2 in LO2 or HepG2 cell line. B and C, 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) analysis of the cell viability after cotransfection with miR-942-3p mimic and MBL2 plasmid or miR-942-3pinhibitor and si-MBL2 in HCC cells. D and E, Transwell analysis of the cell invasive potential after cotransfection of miR-942-3p mimic and MBL2 plasmid or miR-942-3p inhibitor and si-MBL2 in HCC cells. Data were given as mean ± standard error of the mean of 3 experiments. *P< .05; **P< .01.
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