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Fig 1.

Increased UNC50 expression in HCC.

(A) Northern blotting analysis of UNC50 mRNA expression levels in 12 paired HCC tissues (T) and adjacent non-cancerous tissues (N); 28S and 18S bands were used as the references. (B) Real-time PCR analysis of UNC50 expression levels in 44 paired tissues. Relative mRNA expression levels are normalized to β-actin; log2-transformed fold changes of HCC tissues compared to the adjacent non-cancerous tissues were calculated by the comparative cycle threshold (ΔΔCt) method. The paired tissues are ordered from low to high ΔΔCt values. Cutoff values were set to ±1 to identify the significance of changes. (C) Western blotting analysis of UNC50 levels in another 12 paired HCC tissues; β-actin was used as the reference.

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Fig 2.

Confirmation of microarray results in UNC50 overexpression and knockdown Hep3B cells.

(A) Western blotting confirmation of the effectiveness of UNC50 overexpression and knockdown; β-actin served as the reference. (B, C) Real-time PCR confirmation of seven regulated genes in response to UNC50 (B) knockdown or (C) overexpression; expression levels were normalized against β-actin. **: p<0.01.

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Table 1.

List of main regulated genes downstream of the EGFR pathway in UNC50 knockdown Hep3B cells.

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Fig 3.

Western blotting confirmation that UNC50 affects cellular EGFR pathway activity.

Cells (105 from each cell type) were seeded to 24-well plates in DMEM with 10% FBS (Complete medium). After adherence, cells were pre-treated with serum free DMEM for 24 hours before being stimulated with either flesh serum free DMEM, complete medium, or complete medium with 1ng/ml EGF for 8 hours. Lysates were then collected and analyzed for pEGFR, EGFR, β-actin, cyclin D1 and UNC50 by western blot. SF = serum-free DMEM.

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Fig 4.

UNC50 prompts EGF-induced cell cycle entry and proliferation.

(A) Flow cytometry analysis of cells stimulated with complete medium (10% FBS), complete medium with 1 ng/ml EGF (EGF) added for another 24 hours, or 10 μmol/ml erlotinib (Erlotinib) after EGF treatment. (B) MTT evaluation of cell proliferation status. Top: Cells were cultured in complete medium without change of medium; cell vitality was analyzed every 24 hours. Bottom: Cells were cultured in complete medium with 1 ng/ml EGF and replaced with fresh medium every 12 hours to sustain EGF levels. Cell vitality was analyzed every 24 hours. *: p<0.05, **: p<0.01.

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Fig 5.

Flow cytometry and immunofluorescence analyses of EGFR distribution.

(A, B) Cells not treated with 0.05% Triton X-100 before antibody staining, (C, D) Cells permeabilized by 0.05% Triton X-100 before antibody staining. Isotype rabbit immunoglobulin G (IgG) was used as the negative control. (E) Cells were stained for EGFR with Alexa 488-conjugated EGFR antibody and visualized under a fluorescence microscope at 488 nm excitation light. Scale bar is 10 μm.

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Table 2.

Gmh1p interaction partners in yeast.

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Table 2 Expand

Fig 6.

Distribution of recombinant UNC50 protein.

Hep3B cells at approximately 40% confluence were transfected with 1 μg pEGFP-N1-UNC50. After 48-hour transfection, cells were fixed in 4% paraformaldehyde and stained for Golgi apparatus, endoplasmic reticulum, and early endosome markers AKR7A2, calnexin 1, and early endosomal autoantigen 1 (EEA1), respectively. Cells were examined under a fluorescence microscope at corresponding excitation light. Scale bar is 10 μm.

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