Journal: Carcinogenesis

Article Title: A potent hydroxamic acid-based, small-molecule inhibitor A452 preferentially inhibits HDAC6 activity and induces cytotoxicity toward cancer cells irrespective of p53 status.

doi: 10.1093/carcin/bgx121

Figure Lengend Snippet: Figure 2. A452 suppresses the cell growth and viability of CRC cells. (A) HCT116 and (B) HT29 cells were cultured with 0.1% DMSO (control) or the indicated doses of A452 for 72 h, and CCK-8 assays were performed to analyze viability (n = 3). (D) HCT116 and (F) HT29 cells were cultured for 24 h with 0.1% DMSO (control), A452 or SAHA at the indicated concentrations for 24 h. The levels of the indicated proteins were assessed by Western blotting. α-Tubulin is shown as a loading control. The cell growth and viability of HCT116 (C and G) and HT29 (E and H) cells cultured with 0.1% DMSO (control) or A452, SAHA, cisplatin, irinotecan or capecitabine at the indicated con- centrations. Viable cell numbers and viability was measured using a CCK-8 assays (n = 3). (I) Colony formation assays were carried out with HCT116 and HT29 cells for 21 days with a vehicle control (0.1% DMSO) or the indicated concentrations of A452. The quantitative results were obtained by calculating the number of colonies (n = 3). The effect of the HDAC6 knockdown on HCT116 (J) and HT29 (K) cell proliferation. Cell proliferation was monitored for 10 days (240 h) using an IncuCyte ZOOM system in an incubator (5% CO2, at 37°C). Cell proliferation in the cells in which HDAC6 was downregulated was decreased to a comparable degree of A452. Data are expressed as the mean ± SD from three independent experiments (n = 3). *P < 0.05, **P < 0.01 or ***P < 0.001 versus the DMSO control, Student’s t-test.

Article Snippet: The cells were treated with DMSO, suberoylanilide hydroxamic acid (SAHA) (Sigma-Aldrich, St. Louis, MO), ACY-1215, cisplatin, capecitabine, tubastatin A, irinotecan (Selleck Chemicals) or A452 (a γ-lactam based HDAC6 inhibitor) (20), which was kindly provided by Dr. Gyoonhee Han (Yonsei University, Seoul, Korea).

Techniques: Cell Culture, Control, CCK-8 Assay, Western Blot, Knockdown

Journal: Carcinogenesis

Article Title: A potent hydroxamic acid-based, small-molecule inhibitor A452 preferentially inhibits HDAC6 activity and induces cytotoxicity toward cancer cells irrespective of p53 status.

doi: 10.1093/carcin/bgx121

Figure Lengend Snippet: Figure 3. A452 induces apoptosis and DNA damage of CRC cells. (A) HCT116 and (B) HT29 cells were cultured with 0.1% DMSO (control) or A452 (0.5, 1, 2 uM), SAHA (5 uM), cisplatin (10 uM), irinotecan (5 uM), or capecitabine (10 uM) at the indicated concentrations for 24 h. The Western blot analysis shows PARP degradation, proapoptotic and antiapoptotic markers. α-Tubulin is shown as a loading control. (C) HCT116 and (D) HT29 cells were treated with the indicated compounds for 24 h. Caspase-3 activity was determined using the substrate DEVD-pNA; relative caspase-3 activities are the ratio of treated cells to untreated cells (control; n = 3). (E) HCT116 and (F) HT29 cells were treated with the indicated compounds for 48 h and stained with annexin V and PI for 45 min. Apoptosis induced by these compounds was then assessed by flow cytometry (n = 3). Data are expressed as mean ± SD from three independent experiments. *P < 0.05 or **P < 0.01 versus the DMSO control, Student’s t-test.

Article Snippet: The cells were treated with DMSO, suberoylanilide hydroxamic acid (SAHA) (Sigma-Aldrich, St. Louis, MO), ACY-1215, cisplatin, capecitabine, tubastatin A, irinotecan (Selleck Chemicals) or A452 (a γ-lactam based HDAC6 inhibitor) (20), which was kindly provided by Dr. Gyoonhee Han (Yonsei University, Seoul, Korea).

Techniques: Cell Culture, Control, Western Blot, Activity Assay, Staining, Flow Cytometry

Journal: Acta pharmaceutica Sinica. B

Article Title: Carboxylesterase 1 family knockout alters drug disposition and lipid metabolism.

doi: 10.1016/j.apsb.2022.10.017

Figure Lengend Snippet: Figure 5 Mouse Ces1 and human CES1 influence metabolite-to-capecitabine ratios in plasma. Pharmacokinetics of capecitabine and its 4 metabolites (5-DFCR, 5-DFUR, 5-FU and FBAL) after oral administration of capecitabine (500 mg/kg) to female WT, Ces1e/e and TgCES1 mice. (A, B) Plasma 5-DFCR to capecitabine ratio versus time curves and AUC ratios. (C, D) Plasma 5-DFUR to capecitabine ratio versus time curves and AUC ratios. (E, F) Plasma 5-FU to capecitabine ratio versus time curves and AUC ratios. (G, H) Plasma FBAL to capecitabine ratio versus time curves and AUC ratios. Data are presented as mean SD (n Z 4e7; ****P < 0.0001 when compared with WT mice; þP < 0.05; þþP < 0.01 when TgCES1 compared with Ces1e/e mice; the statistical calculation was performed after log-transformation of the data; one-way ANOVA followed by Tukey’s post hoc test).

Article Snippet: The capecitabine (Carbosynth, Berkshire, UK) working solution was 50 mg/mL, including 3% (v/v) DMSO, 4% Tween 80/ ethanol (1:1; v/v) and 40 mmol/L NaAc (pH 4.2).

Techniques: Clinical Proteomics, Drug discovery, Transformation Assay

Journal: International Journal of Cancer

Article Title: Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma

doi: 10.1002/ijc.33916

Figure Lengend Snippet: Number of patients receiving gemcitabine with capecitabine (GEMCAP) or gemcitabine monotherapy (GEM) over time [Color figure can be viewed at wileyonlinelibrary.com ]

Article Snippet: de Jong EJM , Janssen QP , Simons TFA , et al. Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma .

Techniques:

Journal: International Journal of Cancer

Article Title: Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma

doi: 10.1002/ijc.33916

Figure Lengend Snippet: Overall survival, by type of adjuvant chemotherapy. Hazard ratio for death: 0.71 (95% CI: 0.56‐0.90), log‐rank P = .0038*. GEM, gemcitabine monotherapy; GEMCAP, gemcitabine with capecitabin [Color figure can be viewed at wileyonlinelibrary.com ]

Article Snippet: de Jong EJM , Janssen QP , Simons TFA , et al. Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma .

Techniques: Adjuvant

Journal: International Journal of Cancer

Article Title: Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma

doi: 10.1002/ijc.33916

Figure Lengend Snippet: Number of completed chemotherapy cycles in patients treated with gemcitabine with capecitabine (GEMCAP) or gemcitabine (GEM)

Article Snippet: de Jong EJM , Janssen QP , Simons TFA , et al. Real‐world evidence of adjuvant gemcitabine plus capecitabine vs gemcitabine monotherapy for pancreatic ductal adenocarcinoma .

Techniques: