oxaliplatin (o9512)  (Millipore)

Journal: American Journal of Cancer Research

Article Title: Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression

doi: 10.62347/XTRT2780

Figure Lengend Snippet: Establishment and characterization of oxaliplatin-resistant LoVo colorectal cancer cell line. A. Stable oxaliplatin resistance was maintained by exposing colorectal cancer cell lines to oxaliplatin (0-25 μg/mL) for 24 h, which resulted in 50% cell death at 15 μg/mL in colorectal cancer cell lines. The procedure was repeated until a fourfold greater IC50 (60 μg/mL) oxaliplatin resistance was established. B. Distinct morphological characteristics between the LoVoparental and LoVoOXAR cell lines were observed under 20 × magnification. C and D. MTT assay was used to determine the IC50 values of the oxaliplatin-treated LoVoparental and LoVoOXAR colorectal cancer cell lines. The IC50 values of LoVoparental and LoVoOXAR cells were 15 and 60 μg/mL, respectively. The data were expressed mean ± standard deviation (SD, n = 3). *P < 0.05, **P < 0.01, ***P < 0.001 versus ****P < 0.0001 versus control. E. The resistance of the two cell lines to oxaliplatin was compared. *P < 0.05 versus LoVoparental cells and ##P < 0.01 LoVoparental versus oxaliplatin-resistant LoVo cells.

Article Snippet: Oxaliplatin (O9512), 5-FU (F6627), and irinotecan hydrochloride (I1406) were procured from Sigma-Aldrich.

Techniques: MTT Assay, Standard Deviation

Journal: American Journal of Cancer Research

Article Title: Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression

doi: 10.62347/XTRT2780

Figure Lengend Snippet: Ability of chromium (III)-based compound to suppress colorectal cancer cells. A and B. MTT assay was used to determine the IC50 values of LoVoparental and LoVoOXAR colorectal cancer cell lines treated with the chromium (III)-based compound for 24 h. The IC50 values of LoVoparental and LoVoOXAR colorectal cancer cell lines were 500 and 2000 μg/mL, respectively. C. The two cell lines were compared. *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001 versus the control group of LoVoparental, and ##P < 0.01, and ####P < 0.0001 LoVoparental versus LoVoOXAR colorectal cancer cells. D. Clinical drugs were used as follows: oxaliplatin; 20 µg/mL, 5-FU; 20 µg/mL, and irinotecan; 20 µg/mL. The synergetic effect of the chromium (III)-based compound when combined with clinical drugs significantly inhibited the viability of LoVoparental [200 μg/mL chromium (III)-based compound with 5 µg/mL oxaliplatin] and LoVoOXAR [500 μg/mL chromium (III)-based compound with 20 µg/mL oxaliplatin] colorectal cancer cell lines. The clinical drugs that inhibited the development of colorectal cancer cell lines were made more effective by the chromium (III)-based compound. Significance is denoted as *P < 0.05 and ***P < 0.001 versus the control group of LoVoparental cells, and #P < 0.05 and ###P < 0.001 versus the control group of LoVoOXAR cells. E-H. Epithelial-mesenchymal transition markers (E-cadherin and vimentin) were determined using immunofluorescence staining and western blot. GAPDH was used as an internal control. The scale bar was 50 μm. The data were expressed as mean ± standard deviation (SD, n = 3). *P < 0.05, **P < 0.01 versus control group.

Article Snippet: Oxaliplatin (O9512), 5-FU (F6627), and irinotecan hydrochloride (I1406) were procured from Sigma-Aldrich.

Techniques: MTT Assay, Immunofluorescence, Staining, Western Blot, Standard Deviation

Journal: American Journal of Cancer Research

Article Title: Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression

doi: 10.62347/XTRT2780

Figure Lengend Snippet: Inhibition of HCT-116 and SW620 colorectal cancer cell migration by the chromium (III)-based compound. The chromium (III)-based compound inhibited the migration ability of colorectal cancer cells. HCT-116 and SW620 colorectal cancer cells were incubated with the chromium (III)-based compound in a dose-dependent manner for 48 h, and the migration rates were measured by transwell assay. The HCT-116 cells were incubated with the chromium (III)-based compound (IC50 dose at 800 µg/mL), oxaliplatin (IC50 dose at 35 µg/mL), and combination of chromium (III)-based compound and oxaliplatin. The SW620 cells were incubated with the chromium (III)-based compound (IC50 dose at 900 µg/mL), oxaliplatin (IC50 dose at 25 µg/mL), and combination of chromium (III)-based compound and oxaliplatin. The scale bar was 100 μm. The data are shown as the mean ± standard deviation (SD) of three replicates. *P < 0.05, **P < 0.01, and ***P < 0.001 compared with the control group of SW620 cells. #P < 0.05, ##P < 0.01, and ###P < 0.001 compared with the control group of HCT-116 cells.

Article Snippet: Oxaliplatin (O9512), 5-FU (F6627), and irinotecan hydrochloride (I1406) were procured from Sigma-Aldrich.

Techniques: Inhibition, Migration, Incubation, Transwell Assay, Standard Deviation

Journal: American Journal of Cancer Research

Article Title: Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression

doi: 10.62347/XTRT2780

Figure Lengend Snippet: Chromium (III)-based compound-enhanced apoptosis in LoVo oxaliplatin-resistant colorectal cancer cells by activating ER stress pathway. The phosphorylation levels of eIF2α, PERK, ATF4, and CHOP, which are ER-stress protein markers, increased, resulting in an increase in cleaved caspase 3 and a decrease in full-length PARP, ultimately leading to apoptosis. All proteins were analyzed by Western blot. GAPDH was used as an internal control.

Article Snippet: Oxaliplatin (O9512), 5-FU (F6627), and irinotecan hydrochloride (I1406) were procured from Sigma-Aldrich.

Techniques: Western Blot

Journal: American Journal of Cancer Research

Article Title: Novel chromium (III)-based compound for inhibition of oxaliplatin-resistant colorectal cancer progression

doi: 10.62347/XTRT2780

Figure Lengend Snippet: Schematic of chromium (III)-based compound-induced apoptosis in LoVo oxaliplatin-resistant colorectal cancer cells via activation of ER stress pathway.

Article Snippet: Oxaliplatin (O9512), 5-FU (F6627), and irinotecan hydrochloride (I1406) were procured from Sigma-Aldrich.

Techniques: Activation Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Platform combining statistical modeling and patient-derived organoids to facilitate personalized treatment of colorectal carcinoma

doi: 10.1186/s13046-023-02650-z

Figure Lengend Snippet: TGMO-based screen for cell line specific ODCs in CRC 3D complex models. A Initial selection of drugs used in the TGMO-based screen B . Schematic representation of the TGMO platform. Regression coefficients generated from search 3 of single drug 1 st order, drug-drug and single drug 2 nd order drug interactions (red, burgundy and pink lines, respectively) in C 3Dcc SW620 D 3Dcc LS174T (green/orange bars respectively) and the therapeutic window (stripped black bars). E Schematic representation of the generation of complex CRC FOLFOXIRI resistant 3D models, 3D-FX LSFXR and 3D-FX SWFXR and respective ODC identification. F 3D-FX SWFXR and G 3D-FX LSFXR (solid green/orange squared bars respectively) in the left panel. In yellow is highlighted the most robust drug interaction that is maintained in each final ODC. In the corresponding right panels, the activity of the ODCs, corresponding monotherapies (colored bars) and FOLFOXIRI (folinic acid [0.5 µM], 5-FU [10 µM], SN38 [0.1 µM] and oxaliplatin [0.5 µM], red bars) in CRC 3D models, and activity in 3Dcc CCD841 (stripped black bars) used to generate the therapeutic window (TW). Activity is measured by ATP levels vs. CTRL (< 0.15% DMSO). Data are presented as the mean of N = 2–3 independent experiments, error bars represent SD. Significance is determined by one-way ANOVA (regression models, left panel) and two-way ANOVA (activity graphs, right panel) with * p < 0.05, ** p < 0.01 and *** p < 0.001

Article Snippet: Regorafenib (R-8024, 20 mg/mL), vemurafenib (V-2800, 50 mg/mL), erlotinib (E-007, 15 mg/mL), lapatinib (L-4904, 20 mg/mL), Palbociclib (P-7744, 30 mg/mL),, trametinib (T-8188, 15 mg/mL), nilotinib (N-8207,10 mg/mL), olaparib (O-920, 10 mg/mL), BEZ-235 (N-4288, 10 mg/mL) were purchased from LC labs (Woburn, MA, USA); vatalanib (PTK787, 10 mg/mL) from SelleckChem (Houston, Texas, USA); AZD-4547 (HY-13330,10 mg/mL) and SN38 (HY-13704/CS-1579, 1 mg/mL) from MedChemExpress (Monmouth Junction, New Jersey, USA); 5-flurouracil (F6627, 10 mg/mL), folinic acid (F7878, 20 mg/mL), oxaliplatin (O9512, 5 mg/mL in UltraPure distilled water) from Sigma-Aldrich.

Techniques: Selection, Generated, Activity Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Platform combining statistical modeling and patient-derived organoids to facilitate personalized treatment of colorectal carcinoma

doi: 10.1186/s13046-023-02650-z

Figure Lengend Snippet: Cross-validation of ODCs activity on patient-derived organoids. A Schematic representation of our patient-derived organoids platform. B Representative images of PDOs from PCRC-1, PCRC-2 and PCRC-3 treated with ODC LSFXR . Scale bar represents 500 µm C . Activity of all four ODCs, and corresponding monotherapies and FOLFOXIRI (folinic acid [0.5 µM], 5-FU [10 µM], SN38 [0.1 µM] and oxaliplatin [0.5 µM], red bars) in PDOs from PCRC-1 (burgundy bars), PCRC-2 (dark green bars) and PCRC-3 (navy bars). Activity is measured by ATP levels vs. CTRL (< 0.15% DMSO). Data is presented as mean of N = 3 independent experiments, error bars represent SD. Significance is determined by two-way ANOVA with * p < 0.05, ** p < 0.01 and *** p < 0.001

Article Snippet: Regorafenib (R-8024, 20 mg/mL), vemurafenib (V-2800, 50 mg/mL), erlotinib (E-007, 15 mg/mL), lapatinib (L-4904, 20 mg/mL), Palbociclib (P-7744, 30 mg/mL),, trametinib (T-8188, 15 mg/mL), nilotinib (N-8207,10 mg/mL), olaparib (O-920, 10 mg/mL), BEZ-235 (N-4288, 10 mg/mL) were purchased from LC labs (Woburn, MA, USA); vatalanib (PTK787, 10 mg/mL) from SelleckChem (Houston, Texas, USA); AZD-4547 (HY-13330,10 mg/mL) and SN38 (HY-13704/CS-1579, 1 mg/mL) from MedChemExpress (Monmouth Junction, New Jersey, USA); 5-flurouracil (F6627, 10 mg/mL), folinic acid (F7878, 20 mg/mL), oxaliplatin (O9512, 5 mg/mL in UltraPure distilled water) from Sigma-Aldrich.

Techniques: Activity Assay, Derivative Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Platform combining statistical modeling and patient-derived organoids to facilitate personalized treatment of colorectal carcinoma

doi: 10.1186/s13046-023-02650-z

Figure Lengend Snippet: Optimization of patient specific ODCs. A Regression coefficients generated from search 1 of the TGMO-based screen on PDOs, describing single drug 1 st order, drug-drug and single drug 2 nd order drug-drug interactions (red, burgundy and pink lines, respectively) for CRC-1 B . CRC-2 and C . CRC-3 (left panels). In yellow is highlighted the most robust drug-drug interaction in each patient specific ODC. In the corresponding middle panels, activity of the patient specific ODCs, corresponding monotherapies (solid colored bars), and FOLFOXIRI (folinic acid [0.5 µM], 5-FU [10 µM], SN38 [0.1 µM] and oxaliplatin [0.5 µM], red bars) in each PDO and in CCD841 3Dcc (black stripped bars). Activity is measured by ATP levels vs. CTRL (< 0.15% DMSO). Data is presented as mean of N = 3 independent experiments, error bars represent SD. Significance is determined by one-way ANOVA (regression models, left panel) and two-way ANOVA (activity graphs, right panel) with * p < 0.05, ** p < 0.01 and *** p < 0.001. In the right panels, representative images of PDO treated with their corresponding patient specific ODC. Scale bar represents 500 µm

Article Snippet: Regorafenib (R-8024, 20 mg/mL), vemurafenib (V-2800, 50 mg/mL), erlotinib (E-007, 15 mg/mL), lapatinib (L-4904, 20 mg/mL), Palbociclib (P-7744, 30 mg/mL),, trametinib (T-8188, 15 mg/mL), nilotinib (N-8207,10 mg/mL), olaparib (O-920, 10 mg/mL), BEZ-235 (N-4288, 10 mg/mL) were purchased from LC labs (Woburn, MA, USA); vatalanib (PTK787, 10 mg/mL) from SelleckChem (Houston, Texas, USA); AZD-4547 (HY-13330,10 mg/mL) and SN38 (HY-13704/CS-1579, 1 mg/mL) from MedChemExpress (Monmouth Junction, New Jersey, USA); 5-flurouracil (F6627, 10 mg/mL), folinic acid (F7878, 20 mg/mL), oxaliplatin (O9512, 5 mg/mL in UltraPure distilled water) from Sigma-Aldrich.

Techniques: Generated, Activity Assay

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: HDAC class I inhibitor domatinostat sensitizes pancreatic cancer to chemotherapy by targeting cancer stem cell compartment via FOXM1 modulation

doi: 10.1186/s13046-022-02295-4

Figure Lengend Snippet: Domatinostat can sensitize pancreatic cancer cells to chemotherapeutics treatment. CI (combination index) values (mean ± SD from at least three separate experiments performed in quadruplicates) computed at 50% of cell kill (CI 50 ) CalcuSyn software after 96 h. Two schedules of treatment were represented in PANC1, PANC28 and ASPC1 cell lines. Equitoxic doses of drugs with domatinostat administered at same time with chemotherapy (in figure domatinostat CON) and equitoxic doses of drugs with domatinostat administered 24 h before the same chemotherapy (in figure domatinostat SEQ). In A . 5’DFUR, SN-38 and oxaliplatin plus domatinostat combinations were reported, in B . gemcitabine and taxol plus domatinostat combinations were reported. The combinations were considered synergistic when CIs were below 0.9 and additive when CIs were below 1.1 C . -D . DRI (doses reduction index) values (mean ± SD from at least three separate experiments performed in quadruplicates) computed at 50% of cell kill (DRI 50 ) CalcuSyn software after 96 h in PANC1, PANC28 and ASPC1 cells. In C. DRI 50 for 5’DFUR, SN-38 and oxaliplatin plus domatinostat combinations. In D . DRI 50 for gemcitabine and taxol plus domatinostat combinations. E . -F . ASPC1, PANC1 and PANC28 cells were treated for 96 h with increasing concentration of domatinostat alone and in combination with increasing concentration of Gemcitabine/Taxol (GT) (doses are reported in figure). Cell growth expressed as percentage of control was assessed by sulforhodamine B colorimetric assay (see )

Article Snippet: Taxol (#PHL89806), 5′-deoxy-5-fluoro-uridine, (5’DFUR) (#F8791), SN-38 (#sc-203,697), oxaliplatin (#O9512) were purchased from Sigma- Aldrich (St. Louis,MO, USA).

Techniques: Software, Concentration Assay, Colorimetric Assay