Fig 1: Effect of PYGB siRNA on the cell viability of the osteosarcoma cell lines MG63 and HOS. Following transfection with PYGB siRNA, the effect of PYGB siRNA on (A) the cell viability of MG63 cells and (B) the cell proliferation of HOS cells was evaluated by a Cell Counting kit-8 assay for 0, 24, 48 and 72 h. Data are expressed as the mean ± standard deviation (n=3). *P<0.05, **P<0.01 and ***P<0.001 vs. the NC group. Data are expressed as the mean ± standard deviation (n=3). PYGB, Brain type glycogen phosphorylase; NC, negative control; siRNA, small interfering RNA.
Fig 2: PYGB silencing affects the NF-?B/Nrf2 signaling pathway in PC3 cells. (A) Reverse transcription-quantitative polymerase chain reaction was performed to measure the expression levels of NF-?B and Nrf2 in PC3 cells. (B) Western blotting was performed to measure the expression levels of NF-?B and Nrf2 in PC3 cells. **P<0.01, ***P<0.001 vs. mock group. No significant differences were detected between the control and mock groups. PYGB, brain-type glycogen phosphorylase; NF-?B, nuclear factor-?B; Nrf2, nuclear factor-erythroid 2-related factor 2; si-/siRNA, small interfering RNA.
Fig 3: PYGB silencing modulates the expression levels of Bax and Bcl-2 in PC3 cells. PC3 cells were transfected with the siRNA negative control (mock group) and PYGB siRNA (si-PYGB group). The cells in control group received no treatment. (A) Reverse transcription-quantitative polymerase chain reaction and (B) western blotting were carried out to detect the mRNA and protein expression levels of Bax and Bcl-2, respectively, in PC3 cells transfected with the siRNA negative control (mock group) and PYGB siRNA (si-PYGB group); the control group was untreated. **P<0.01 vs. mock group. No significant differences were detected between the control and mock groups. PYGB, brain-type glycogen phosphorylase; Bcl-2, B-cell lymphoma-2; Bax, Bcl-2-associated X protein; si-/siRNA, small interfering RNA.
Fig 4: Brain-type glycogen phosphorylase was upregulated in human gastric cancer. A, Brain-type glycogen phosphorylase level in GC tissues and in normal tissues were analyzed by qRT-PCR (57 pairs of gastric cancer and nontumor tissues). B, Brain-type glycogen phosphorylase protein levels were determined by immunoblot. C, Immunohistochemistry assay detected upregulated PYGB expression level in GC tissue samples. D, Correlation between overall survival rates and PYGB expression level. E, Relative PYGB expression level in several gastric cancer cell line: HGC-27, SNU-1, AGS, and MKN45, and normal gastric epithelia cell line GES-1 quantified by qRT-PCR (mean ± SD, **P < .01). GC indicates gastric cancer; PYGB, brain-type glycogen phosphorylase; qRT-PCR, quantitative real-time polymerase chain reaction; SD, standard deviation.
Fig 5: PYGB promoted the migration and invasion of gastric cancer cells. A and B, Scratch assays (A) and transwell assays (B) were performed to detect cell migration and cell invasion in control or PYGB knockdown AGS and MKN45 cells. (Scale bar: 200 µm in panel A; 100 µm in panel B; mean ± SD, *P < .05; **P < .01). PYGB indicates brain-type glycogen phosphorylase.
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