Journal: Oncology Reports

Article Title: Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells

doi: 10.3892/or.2024.8730

Figure Lengend Snippet: List of antibodies.

Article Snippet: Glo1 , Proteintech Group, Inc. , 15140-1-AP.

Techniques:

Journal: Oncology Reports

Article Title: Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells

doi: 10.3892/or.2024.8730

Figure Lengend Snippet: The effects of NaB on the activation of PERK and Nrf2. (A) DU145 cells were treated with NaB (2.5 or 5 mM) for 48 h, the PERK expression was determined. (B) The changes of Nrf2 expression and the cell viability were examined in cct020312 and NaB-treated cells. (C) After the cells treated with NaB for 24 h, the levels of cytoplasmic and nuclear Nrf2 and Bach1 were determined. (D) The distribution of Nrf2 in cytoplasm and nuclei in DU145 cells was evaluated by immunofluorescence assay. (E) The DU145 cells were incubated with AI-1 (50 µM) for 2 h followed by treatment with NaB for another 48 h, then the expression of Nrf2 and Glo1 was determined. Results are expressed as the mean ± SEM. *P<0.05, **P<0.01 and ***P<0.001 vs. the Control group; # P<0.05 vs. respective NaB-treated alone cells. NaB, sodium butyrate; PERK, eukaryotic translation initiation factor 2 alpha kinase 3; Nrf2, nuclear factor erythroid 2-related factor 2; Bach1, BTB domain and CNC homolog 1; Glo1, glyoxalase1.

Article Snippet: Glo1 , Proteintech Group, Inc. , 15140-1-AP.

Techniques: Activation Assay, Expressing, Immunofluorescence, Incubation, Control

Journal: Oncology Reports

Article Title: Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells

doi: 10.3892/or.2024.8730

Figure Lengend Snippet: The effects of NaB on Stat1, JAK2 and Stat3 expression. (A) DU145 cells were treated with NaB (2.5 or 5 mM) for 48 h and the expression of these genes was determined. (B) The DU145 cells were incubated with ruxolitinib (0.5 µM) for 2 h followed by treatment with NaB for 48 h, the expression of p-Stat3 and Glo1 was determined. (C) The relative ROS was measured in cells treated with NaB (2.5 or 5 mM) for 48 h. (D) After the cells were incubated with NAC (5 mM) or medium for 2 h followed by treatment with NaB for another 48 h, the protein level of p-Stat3 was determined in various groups. (E and F) Cells were pretreated with Colivelin (10 µM) or medium for 2 h followed by treatment with NaB for another 48 h. Then, the expression of the (E) target genes and (F) MG-H1 production were determined. Results are expressed as the mean ± SEM. *P<0.05, **P<0.01 and ***P<0.001 vs. the Control group; # P<0.05, ## P<0.01 and ### P<0.001 vs. respective NaB-treated alone cells. NaB, sodium butyrate; Stat, signal transducer and activator of transcription; JAK2, Janus kinase 2; Glo1, glyoxalase1; ROS, reactive oxygen species; NAC, N-acetyl-cysteine; MG-H1, hydroimidazolone; Nrf2, nuclear factor erythroid 2-related factor 2; HO-1, heme oxygenase-1; p-, phosphorylated.

Article Snippet: Glo1 , Proteintech Group, Inc. , 15140-1-AP.

Techniques: Expressing, Incubation, Control

Journal: Oncology Reports

Article Title: Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells

doi: 10.3892/or.2024.8730

Figure Lengend Snippet: The effects of MGO, Glo1, Stat3 and CaMKII phosphorylation on NaB-mediated target gene expression and cell viability. (A) After treatment with MGO (0.2-1.6 mM) for 48 h, the expression of Nrf2, Glo1 and HO-1, as well as the cell viability were determined. (B) The cell viability of the DU145 cells with overexpression of Glo1 or Stat3 was examined. (C) Cells were pretreated with KN-93 (10 µM) for 2 h followed by treatment with NaB for 48 h. Then, the expression of MAPKs and pro-apoptotic proteins were determined. Results are expressed as mean ± SEM. *P<0.05, **P<0.01 and ***P<0.001 vs. the Vector or Control group; # P<0.05, ### P<0.001 vs. respective NaB-treated alone cells. MGO, methylglyoxal; Glo1, glyoxalase1; Stat3, signal transducer and activator of transcription 3; CaMKII, calcium/calmodulin dependent protein kinase II gamma; NaB, sodium butyrate; Nrf2, nuclear factor erythroid 2-related factor 2; HO-1, heme oxygenase-1; PARP, Poly (ADP-Ribose) polymerase.

Article Snippet: Glo1 , Proteintech Group, Inc. , 15140-1-AP.

Techniques: Phospho-proteomics, Targeted Gene Expression, Expressing, Over Expression, Plasmid Preparation, Control

Journal: Oncology Reports

Article Title: Butyrate increases methylglyoxal production through regulation of the JAK2/Stat3/Nrf2/Glo1 pathway in castration‑resistant prostate cancer cells

doi: 10.3892/or.2024.8730

Figure Lengend Snippet: Effects of KN-93 on cell proliferation the effects of NaB on normal RWPE-1 cells. (A) The relative cell proliferation of DU145 cells and the expression of c-Myc and cyclin D1 were evaluated in NaB (5 mM) alone, and co-treatment with KN-93, NAC, or Colivelin for indicated time. (B) The cell viability and the levels of Glo1 and Stat3 in RWPE-1 cells were examined after treatment with NaB for 48 h. Results are expressed as the mean ± SEM. **P<0.01 and ***P<0.001 vs. the Control group. (C) The proposed schematic diagram of NaB-mediated Nrf2/Glo1/MGO pathway and apoptosis in PCa cells. NaB inhibits the expression and activity of Nrf2 through PERK inactivation and accumulation of nuclear Bach1. Then, Glo1expression is attenuated via suppression of Janus kinase 2/Stat3 pathway, leading to accumulation of MGO and apoptotic cell death. The elevated MGO further downregulates Nrf2, Glo1 and HO-1. The CaMKII-mediated activation of MAPKs and Stat1 also contributes to NaB-induced cell death. NaB, sodium butyrate; NAC, N-acetyl-cysteine; Glo1, glyoxalase1; Stat3, signal transducer and activator of transcription 3; Nrf2, nuclear factor erythroid 2-related factor 2; MGO, cytotoxic methylglyoxal; PERK, eukaryotic translation initiation factor 2 alpha kinase 3; Bach1, BTB domain and CNC homolog 1; HO-1, heme oxygenase-1; CaMKII, calcium/calmodulin dependent protein kinase II gamma.

Article Snippet: Glo1 , Proteintech Group, Inc. , 15140-1-AP.

Techniques: Expressing, Control, Activity Assay, Activation Assay