Journal: Cell communication and signaling : CCS

Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.

doi: 10.1186/s12964-022-01007-x

Figure Lengend Snippet: Fig. 1 BMX, TMZ, oxaliplatin (Oxp) and doxorubicin (Dox) combination inhibited cell proliferation in CRC cells. (A) The proliferation of BMX, TMZ, Oxp, Dox, BMX plus TMZ, BMX plus Oxp or BMX plus Dox in HT29, HCT116 and RKO cells with various drug concentration. (B) Colony formation capability assay with different treatments of BMX, TMZ, Oxp, BMX plus TMZ, and BMX plus Oxp in HT29, HCT116 and RKO cells; the colonies were counted for quantification. (C) Cell cycle analysis after 48 h treatment with different concentrations of BMX alone or BMX combined with TMZ in HT29, HCT116, and RKO cells and the proportion of cells in each cell cycle phase. SubG1, cell with polyploid chromosome; > 4 N, polyploid cell. (D) Apoptosis analysis after 48 h treatment with different concentrations of BMX alone or BMX combined with TMZ and the apoptotic rate of cells in HT29, HCT116, and RKO cells. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 vs. control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)

Article Snippet: The cell proliferation of CRC cells was measured by CCK8 assay (Targetmol, Shanghai, China).

Techniques: Concentration Assay, Cell Cycle Assay, Control

Journal: Cell communication and signaling : CCS

Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.

doi: 10.1186/s12964-022-01007-x

Figure Lengend Snippet: Fig. 5 BMX, VPA, SAHA, TMZ, Oxp, and Dox combination inhibited cell proliferation in CRC cells. (A) HDAC8 mRNA expression levels stimulated with BMX (5 µM), VPA (4 mM), SAHA (2 µM) with or without TMZ were determined using qRT-PCR assays. (B) HT29, HCT116, and RKO cells were treated with BMX with or without TMZ for 48 h. Then, cells were harvested for detection of acetyl-histone H3 (Lys9/Lys14), acetyl-histone H4 (Lys8), and HDAC8 by Western blot analysis. (C) The proliferation of BMX, VPA, SAHA with or without TMZ, Oxp (5 µM) and Dox (1 µM) in HT29, HCT116, and RKO cells with treatment durations were assayed using the CCK-8 method. (D) Colony formation capability assay with different treatments of BMX, VPA, SAHA with or without TMZ, Oxp and Dox in HT29, HCT116, and RKO cells; the colonies were counted for quantification. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 versus control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)

Article Snippet: The cell proliferation of CRC cells was measured by CCK8 assay (Targetmol, Shanghai, China).

Techniques: Expressing, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Control

Journal: Cell communication and signaling : CCS

Article Title: BMX, a specific HDAC8 inhibitor, with TMZ for advanced CRC therapy: a novel synergic effect to elicit p53-, β-catenin- and MGMT-dependent apoptotic cell death.

doi: 10.1186/s12964-022-01007-x

Figure Lengend Snippet: Fig. 7 Autophagy expression levels stimulated with BMX and PCI-34051 in the presence or absence of TMZ. (A) HT29, HCT116, and RKO cells were treated with BMX and PCI-34051 with or without TMZ for 48 h. Then, cells were harvested for detection of acetyl-histone H3 (Lys9/Lys14), acetyl-histone H4 (Lys8), and HDAC8 by Western blot analysis. (B) The proliferation of BMX and PCI-34051 with or without TMZ in HT29, HCT116, and RKO cells. (C) Colony formation capability assay with different treatments of BMX and PCI-34051 with or without TMZ in HT29, HCT116, and RKO cells; the colonies were counted for quantification. (D, E) Expressions of cleaved caspase 3, cleaved PARP, LC3 and p62 proteins in HT29, HCT116, and RKO cells treated with BMX and PCI-34051 with or without TMZ for 48 h. All results are shown as mean ± s.d. from three independent experiments. *p < 0.05, **p < 0.01, ***p < 0.001 versus control (HT29 cells); #p < 0.05, ##p < 0.01, ###p < 0.001 versus control (HCT116 cells); †p < 0.05, ††p < 0.01, †††p < 0.001 versus control (RKO cells)

Article Snippet: The cell proliferation of CRC cells was measured by CCK8 assay (Targetmol, Shanghai, China).

Techniques: Expressing, Western Blot, Control

Journal: Arthritis Research & Therapy

Article Title: Sirt3 improves monosodium urate crystal-induced inflammation by suppressing Acod1 expression

doi: 10.1186/s13075-023-03107-6

Figure Lengend Snippet: MSU crystals stimulation reduced the expression and deacetylation activity of Sirt3. a Sirt3 mRNA and protein levels were detected in PBMCs of health controls (HC), patients with acute gout (AG), and intermittent gout (IG). Sirt3 mRNA detection (HC, n = 24), (AG, n = 24), (IG, n = 24); GAPDH was used as an internal reference. Sirt3 protein detection (HC, n = 6), (AG, n = 6), (IG, n = 6), TUBULIN as an internal reference. b BMDMs were respectively stimulated with C16:0, MSU, or C16:0 + MSU for 12 h and Western blot was used to detect Sirt3 protein expression. c The protein levels of Sirt3 in the mouse paw treated with MSU crystals or vehicle. Data presented as mean ± SD ( n = 5 mice per group). * P < 0.05. NS means no statistical difference. d Sirt3 agonists (Viniferin) inhibited the acetylation level of mitochondrial proteins in BMDMs treated with Viniferin (1 μM) and C16:0 + MSU crystals for 12 h. Acetyl-conjugated proteins in mitochondrial proteins were blotted with acetylated-lysine antibody. e Viniferin treatment decreased K68 lysine acetylation of mitochondrial SOD2 protein and mitochondrial proteins were analyzed by Western blot in BMDMs. f The activity of SOD in the mitochondrial proteins of BMDMs was detected with WST-8 method. Data are mean ± SD. Three independent repetitive experiments were conducted for each result. *P < 0.05. NS represents P > 0.05

Article Snippet: HY-133987, Mito-TEMPO, and Viniferin were purchased from MedChemExpress (MCE).

Techniques: Expressing, Activity Assay, Western Blot

Journal: Oncology Reports

Article Title: TNF-α promotes the malignant transformation of intestinal stem cells through the NF-κB and Wnt/β-catenin signaling pathways

doi: 10.3892/or.2020.7631

Figure Lengend Snippet: Effects of inhibitors of the NF-κB and Wnt/β-catenin pathways on their activities in TNF-α-induced NCM460s cells. NCM460s cells were respectively incubated with 1, 10, 100 µM of (A) PDTC or (B) IWP-2 without or with 1 ng/ml TNF-α for 3 h. Western blotting was used to analyze the protein expression of genes related with NF-κB and Wnt/β-catenin signaling in the total cell extracts and the nuclear/cytoplasmic extracts. TNF, tumor necrosis factor; NCM460s, NCM460 spheroid; PDTC, pyrrolidine dithiocarbamate; IKKα/β, IκB kinase complex α/β; GSK, glycogen synthase kinase.

Article Snippet: The NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC; cat. no. M4005) and Wnt inhibitor IWP-2 (cat. no. M2237) were purchased from Abmole (Abmole Bioscience, Inc.).

Techniques: Incubation, Western Blot, Expressing