Journal: Molecular cancer research : MCR

Article Title: ECM Composition and Rheology Regulate Growth, Motility and Response to Photodynamic Therapy in 3D Models of Pancreatic Ductal Adenocarcinoma

doi: 10.1158/1541-7786.MCR-16-0260

Figure Lengend Snippet: (1) Initial formation of attachment-free spheroids on agarose beds for 12 days; (2) transplantation and embedding of spheroids in rheologically characterized Matrigel or COL1 ECMs; (3) Longitudinal and terminal (immunofluorescence) imaging of growth and ECM invasion; (4) Treatment with chemotherapy (oxaliplatin) or PDT; and (5) Imaging-based assesment of therapeutic response, co-registered with phenotype.

Article Snippet: Increasing concentrations of oxaliplatin and/or gemcitabine (Tocris; Bristol, UK) were added to each cell type in regular media over the course of approximately 25 passages until a stable proliferative phenotype without chemotherapy was observed and maintained following cryopreservation and thawing.

Techniques: Transplantation Assay, Immunofluorescence, Imaging, Clinical Proteomics

Journal: Molecular cancer research : MCR

Article Title: ECM Composition and Rheology Regulate Growth, Motility and Response to Photodynamic Therapy in 3D Models of Pancreatic Ductal Adenocarcinoma

doi: 10.1158/1541-7786.MCR-16-0260

Figure Lengend Snippet: (A) Representative PANC1 spheroids treated with either chemotherapy or PDT doses notes and stained with calcein (green) and ethidium bromide (red), showing viability of core spheroid cells and ECM infiltrating cells. (B) Dose response, evaluated via MTS, of PANC1 to oxaliplatin or PDT in monolayer, used to inform dose selection for each therapy. The LD90 dose (arrow) of each is selected for subsequent comparison of therapies across contrasting ECM conditions. (C) Dose response (normalized residual volume from image segmentation) for primary spheroids shows modest growth inhibition of primary nodule by oxaliplatin, but n.s. for PDT. (D) Dose response for invading cells (analysis applicable for COL1 only) shows no response to oxaliplatin, approximately 50% killing from PDT at 25 J/cm2 (P <0.01). (E) Further analysis of individual invading cell viability with respect to radial distance from COL1 spheroid edge showing clear separation of PDT and chemotherapy response. (F) Breakdown of response in leading (d > 200 μm) and lagging invaders for chemotherapy and PDT shows further enhancement in PDT response for leading cells.

Article Snippet: Increasing concentrations of oxaliplatin and/or gemcitabine (Tocris; Bristol, UK) were added to each cell type in regular media over the course of approximately 25 passages until a stable proliferative phenotype without chemotherapy was observed and maintained following cryopreservation and thawing.

Techniques: Staining, Selection, Comparison, Inhibition

Journal: Molecular cancer research : MCR

Article Title: ECM Composition and Rheology Regulate Growth, Motility and Response to Photodynamic Therapy in 3D Models of Pancreatic Ductal Adenocarcinoma

doi: 10.1158/1541-7786.MCR-16-0260

Figure Lengend Snippet: (A) Workflow for experiments with chemoresistant sublines (Figures 4 through ​through6),6), (B) Confirmation of resistance to oxaliplatin from comparative dose response in PANC1 and oxaliplatin resistant subline, PANC1OR (top), and for BxPC3 and its oxaliplatin resistant subline, BxPC3OR (bottom). (C) Immunofluorescence and quantification show increased vimentin, decreased E-cadherin in resistant versus non-resistant cells, in a similar trend to invading versus non-invading in above experiments. (D) Measurement of above markers via Western blot quantified at right and normalized to GAPDH.

Article Snippet: Increasing concentrations of oxaliplatin and/or gemcitabine (Tocris; Bristol, UK) were added to each cell type in regular media over the course of approximately 25 passages until a stable proliferative phenotype without chemotherapy was observed and maintained following cryopreservation and thawing.

Techniques: Immunofluorescence, Western Blot

Journal: Molecular cancer research : MCR

Article Title: ECM Composition and Rheology Regulate Growth, Motility and Response to Photodynamic Therapy in 3D Models of Pancreatic Ductal Adenocarcinoma

doi: 10.1158/1541-7786.MCR-16-0260

Figure Lengend Snippet: (A) Comparison of response to oxaliplatin in PANC1 and PANC1OR 3D cultures shows that resistance to low doses of oxaliplatin is preserved in 3D growth conditions, as expected. (B) PDT response of PANC1 and PANC1OR, shows dramatic increase in sensitivity in the latter. (C) Representative images of PDT response in PANC1 and PANC1OR 3D cultures stained with vital dyes. Scalebars = 100 μm.

Article Snippet: Increasing concentrations of oxaliplatin and/or gemcitabine (Tocris; Bristol, UK) were added to each cell type in regular media over the course of approximately 25 passages until a stable proliferative phenotype without chemotherapy was observed and maintained following cryopreservation and thawing.

Techniques: Comparison, Staining

Journal: Molecular cancer research : MCR

Article Title: ECM Composition and Rheology Regulate Growth, Motility and Response to Photodynamic Therapy in 3D Models of Pancreatic Ductal Adenocarcinoma

doi: 10.1158/1541-7786.MCR-16-0260

Figure Lengend Snippet: (A) Immunofluorescence images of PANC1, PANC1 + TGFβ, BxPC3, and BxPC3 + fibroblast conditioned media (FCM) show characteristic increased scattering and loss of adherens junctions in EMT-inducing conditions. (B) Quantification of immunofluorescence at left. (C) Dose response comparison in PANC1 +/− TGFβ for oxaliplatin (top) and PDT (bottom) showing expected chemoresistance but not an enhancement in PDT response as seen in 3D ECM-invading cells. (D) Dose response comparison in BxPC3 and BxPC3 + FCM for oxaliplatin (top) and PDT (bottom). (E) PDT dose response for oxaliplatin-resistant cell lines.

Article Snippet: Increasing concentrations of oxaliplatin and/or gemcitabine (Tocris; Bristol, UK) were added to each cell type in regular media over the course of approximately 25 passages until a stable proliferative phenotype without chemotherapy was observed and maintained following cryopreservation and thawing.

Techniques: Immunofluorescence, Comparison

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pyrotinib targeted EGFR/GRP78 mediated cell apoptosis in high EGFR gene copy number gastric cancer

doi: 10.1186/s13046-025-03485-6

Figure Lengend Snippet: Pyrotinib combined with oxaliplatin exerts synergistic effects in EGFR- high CN gastric cancer. A . Drug synergy maps of SNU719 and NUGC4 cells were plotted by Combenefit software (V2.021). Bliss synergy scores were calculated for oxaliplatin (OXA) and Pyr after 48 h. One representative experiment out of 3 independent experiments is shown. B . Quantitative analysis of EdU positive in SNU719 and NUGC4 cells treated with Pyr (1 µM) or/and OXA (1 µg/ml) for 24 h. C . Quantitative analysis of Annexin V-FITC/PI staining after the indicated treatment. D . Quantitative analysis of cell cycle distribution in SNU719 and NUGC4 cells after the indicated treatment. E . Schematic diagram of the protocol for the animal model experiments. F . Tumor volume curves were plotted every 2 days after indicated treatment ( n = 8). G - H . Tumor weight ( G ) and maximum diameter ( H ) were recorded after excision from xenograft models. Significance was determined by Paired t-test ( F ) and ( B , C , G ) One-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001

Article Snippet: Dacomotinib (HY-13272), afatinib (HY-10261), pyrotinib (HY-104065), oxaliplatin (HY-17371), MG132 (HY-13259), SAL003 (HY15869) were purchased from MedChemExpress (New Jersey, USA) respectively.

Techniques: Software, Staining, Animal Model

Journal: Journal of Experimental & Clinical Cancer Research : CR

Article Title: Pyrotinib targeted EGFR/GRP78 mediated cell apoptosis in high EGFR gene copy number gastric cancer

doi: 10.1186/s13046-025-03485-6

Figure Lengend Snippet: Pyrotinib enhances oxaliplatin chemosensitivity through GRP78 inhibition. A . Western blot analysis revealed differential expression of DNA double-strand break repair proteins (γ-H2A.X) and GRP78 in NUGC4 and SNU719 cells treated with DMSO, Pyr (1 µM), or/and OXA (2.5 µM) for 24 h. B . The expression of GRP78 protein in SNU719 and NUGC4 cells transfected with si NC or si GRP78 . C . CCK-8 cytotoxicity assays demonstrated enhanced OXA sensitivity in GRP78 silenced SNU719 and NUGC4 cells. D . The expression of GRP78 protein in SNU719 and NUGC4 cells transfected with MOCK or OE GRP78 plasmid. E . GRP78 overexpressing GC cells exhibited OXA resistance in CCK-8 assays, showing higher viability than control cells. F - G . Immunofluorescence staining ( F ) and analysis ( g ) showed that after stimulation by OXA (2.5 µM) for 24 h, the γ-H2A.X foci in SNU719 and NUGC4 cell nucleus distinguished in MOCK and OE GRP78 groups. Blue background indicates DAPI, red dots indicate γ-H2A.X foci. Bars, 40 μm. H . Schematic diagram display that Pyr promotes EGFR-GRP78 complex formation in the ER lumen, subsequently activating the PERK/eIF2α/ATF4/CHOP signaling pathway, and finally resulted in the tumor apoptosis in EGFR-high CN GC. Besides, Pyr could sensitize GC cells to OXA by inhibiting GRP78 phosphorylation at T62 which results in GRP78 ubiquitination. Significance between groups was determined by ( C , E ) Paired t-test and ( G ) One-way ANOVA. * p < 0.05; **p < 0.01; *** p < 0.001

Article Snippet: Dacomotinib (HY-13272), afatinib (HY-10261), pyrotinib (HY-104065), oxaliplatin (HY-17371), MG132 (HY-13259), SAL003 (HY15869) were purchased from MedChemExpress (New Jersey, USA) respectively.

Techniques: Inhibition, Western Blot, Quantitative Proteomics, Expressing, Transfection, CCK-8 Assay, Plasmid Preparation, Control, Immunofluorescence, Staining, Phospho-proteomics, Ubiquitin Proteomics

Journal: Journal of neurophysiology

Article Title: Orexin (hypocretin) effects on constitutively active inward rectifier K+ channels in cultured nucleus basalis neurons.

doi: 10.1152/jn.01222.2003

Figure Lengend Snippet: FIG. 4. Pertussis toxin (PTX) sensitivity of OXA (3 M) and [D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO; 3 M) effects on KIR channels. Whole cell voltage-clamp recordings were performed using patch pipettes containing GTP (0.2 mM). [K]o 10 mM. Holding potential was –84 mV. A: comparison of the PTX sensitivity of the OXA-suppressed conductance in NB neurons. NB cultures were selected that displayed a consistent, but smaller OXA response than the cultures found in Fig. 2A, which is advantageous in that if the OXA effect is indeed PTX-sensitive, the toxin may more readily abolish the OXA effect. NB cultures were incubated for 15–20 h in 250 ng/ml of heat-inactivated PTX (Control) or active PTX. The OXA-suppressed con- ductance was calculated as the difference between the resting conductance and the conductance during maximal OXA effect (approximated as the average during the 12-s interval immediately following OXA application). B: compar- ison of the PTX sensitivity of the DAMGO-induced conductance in HEK293A cells. HEK293A cells were transfected with mu opioid receptor (MOR), G protein–coupled inward rectifier K (GIRK)1, GIRK2, and GFP cDNA. Cells were treated with 250 ng/ml of heat-inactivated PTX or active PTX. On each experimental day, the potency of PTX after 11–14 h of treatment was tested in HEK293A cells, before proceeding to the orexin-related, PTX sensitivity experiments. Peptides were applied through pressure ejection. Conductance decrease (A) and increase (B) are represented as a percent, relative to the average resting conductance during the 12-s interval immediately prior to OXA application. Error bars represent SE. *Significant difference at P 0.05 (t-test).

Article Snippet: The following concentrations of drugs were used: OXA (3 M, Peptides International) and [D-Ala2, N-Me-Phe4, Gly-ol5]-enkephalin (DAMGO; 3 M, Bachem).

Techniques: Comparison, Incubation, Control, Transfection

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A and B) Representative deconvoluted epifluorescence images of HCT116 (A) and U2OS (B) cells expressing FBL-GFP (green) and NPM1-RFP (red) from their endogenous loci after 4 h treatments with the indicated amount of drugs. (C) Quantification of the changes in nucleolar eccentricity (x axis) and nucleolar area (y axis; normalized to untreated) in HCT116 and U2OS cells treated with the indicated amounts of drugs, measured using the nucleolar marker NPM1. Plot markers represent median values and error bars median deviation. At least 582 nucleoli per condition and cell line were quantified (see for details). (D) Representative plots showing nucleolar surface contour fluctuations over time in U2OS cells after treatment with 0 or 10 uM oxaliplatin (Ox) for 4 h. Color of traces represent different time points as specified in the legend. (E) Quantification of the changes in NPM1 surface tension in response to drug treatments. Horizontal lines depict median values, boxes the 25th to 75th percentiles, and error bars the 5th to 95th percentiles. n = 136 (untreated), 200 (10 μM cisplatin [Cis]), 217 (100 μM Cis), 178 (10 μM Ox), 167 (100 μM Ox), and 40 (1 μM ActD). See for statistics. (F and G) Phase diagrams showing changes in the dilute and dense-phase concentrations (in arbitrary units [AU]) of FBL-GFP (F) and NPM1-RFP (G) in HCT116 cells treated with increasing concentrations of oxaliplatin and cisplatin. Shaded areas indicate approximate two-phase regimes in which FBL-GFP and NPM1-RFP exist in condensates. Plot markers represent median values and error bars median deviation. At least 268 nucleoli per condition and cell line were quantified (see for details). (H) Changes in FBL and NPM1 transfer energies (∆∆G tr ) in HCT116 and U2OS cells treated with the indicated amounts of cisplatin (blue shades), oxaliplatin (red shades), and actinomycin D (orange shades) for 4 h (relative to untreated HCT116 and U2OS cells). The arrows indicate clinical concentrations of cisplatin and oxaliplatin. Plot markers represent median values and error bars median deviation. At least 268 nucleoli per condition and cell line were quantified (see for details).

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Expressing, Marker

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A and B) Representative deconvoluted epifluorescence images of immunostained SURF6 (green) in HCT116 (A) and U2OS (B) cells expressing NPM1-RFP (red) from its endogenous locus after 4 h treatments with the indicated amount of drugs. (C) Phase diagrams showing changes in the dilute and dense-phase concentrations (in AU) of SURF6 in HCT116 cells treated with increasing concentrations of oxaliplatin and cisplatin. Shaded areas indicate approximate two-phase regimes in which SURF6 exists in condensates. Plot markers represent median values and error bars median deviation. At least 268 nucleoli per condition and cell line were quantified (see for details). (D) Changes in SURF6 and NPM1 transfer energies (∆∆G tr ) in HCT116 and U2OS cells treated with the indicated amounts of cisplatin (blue shades), oxaliplatin (red shades), and actinomycin D (orange shades) for 4 h (relative to untreated HCT116 and U2OS cells). The arrows indicate clinical concentrations of cisplatin and oxaliplatin. Plot markers represent median values and error bars median deviation. At least 268 nucleoli per condition and cell line were quantified (see for details).

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Expressing

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A) Representative confocal images of NPM1-RFP (red) expressing U2OS cells immunostained for the nucleolar rim and cell proliferation marker KI67 (green) after 4 h treatments with the indicated amount of drugs. (B) Quantification of nucleolar KI67 enrichment (y axis), nucleolar eccentricity (x axis) and nucleolar area (plot marker size) in oxaliplatin-treated cells. At least 20 nucleoli per condition were analyzed. See for statistics. (C) Quantification of nucleolar KI67 enrichment in oxaliplatin-, cisplatin- and actinomycin D-treated cells. Horizontal lines depict median values, boxes the 25th to 75th percentiles, and error bars the 5th to 95th percentiles. At least 15 nucleoli per condition were analyzed. See for statistics. (D) Live cell imaging of nucleolar dynamics during mitosis in control and oxaliplatin-treated U2OS cells expressing NPM1-RFP from its endogenous locus. (E) Quantification of cell number during live cell imaging of control and drug-treated cells for 24 h. At least 92 cells per replicate were tracked over time (see for details).

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Expressing, Marker, Live Cell Imaging, Control

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A) Transcript levels of pre- and mature rRNA levels in U2OS knockin cells after treatment with the indicated amounts of drugs for 4 h, measured by qRT-PCR. Black horizontal lines indicate median values, boxes the the 25th to 75th percentiles, and error bars the 5th to 95th percentiles. Gray shading of data points represents technical replicates are shaded in gray according to. (B) Representative confocal images of RNA-FISH stainings against the 45S pre-rRNA (green) in U2OS knockin cells expressing NPM1-RFP (red) from its endogenous locus. The cells were treated with the indicated amounts of drugs for 4 h prior to staining. Image levels were individually adjusted to highlight morphological phenotypes. (C and D) Multi-channel three-dimensional (3D) reconstructions of a representative nucleoli in cells left untreated (C) or treated with 10 μM oxaliplatin for 4 h (D). (E and F) Quantification of the decline in 45S pre-rRNA signal and NPM1 eccentricity over time in U2OS knockin cells treated with the indicated amounts of drugs over time. Plot markers represent median values and error bars median deviation. At least 106 nucleoli per condition and time point were quantified in raw images (see for details).

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Knock-In, Quantitative RT-PCR, Expressing, Staining

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A) Scheme and representative epifluorescence images showing 5-EU incorporation into newly synthesized RNAs in U2OS cells after treatment with the indicated drugs. (B) Quantification of mean nucleolar 5-EU signals and nucleolar eccentricity in U2OS cells treated as in (A). Horizontal lines depict median values, boxes the 25th to 75th percentiles, and error bars the 5th to 95th percentiles. At least 713 nucleoli per condition were quantified. See for statistics. (C) Scheme and representative epifluorescence images showing 5-EU incorporation in U2OS cells during drug treatments for the indicated times. (D) Quantification of changes in nucleolar eccentricity (x axis) and mean nucleolar 5-EU signals (y axis) over time in U2OS cells treated with the indicated drugs. 5-EU signals are normalized to the earliest nucleolar 5-EU measurement (30 min) in untreated cells. Color shades represent different time points. Dashed lines join data points to help visualization. Plot markers represent median values and error bars median deviation. At least 771 nucleoli per treatment and time point were quantified. See for statistics. (E) Quantification of changes in nucleoplasmic (x axis) and mean nucleolar 5-EU signals (y axis) over time. Dashed lines indicated one-phase association fits for oxaliplatin and linear fits for untreated, cisplatin- and actinomycinD-treated U2OS cells. 5-EU signals are normalized to the earliest cytoplasmic 5-EU measurement (30 min) in untreated cells. Plot markers represent median values and error bars median deviation. At least 771 nucleoli per treatment and time point were quantified. See for statistics.

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Synthesized

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A and B) Gel shift assays to detect the dose-dependent cross-linking of recombinant FBL (A) and NPM1 (B) by oxaliplatin (Ox) and cisplatin (Cis) visualized by immunoblotting. Labels mark platinated (+Pt) FBL and NPM1. Asterisks denote unspecific bands. Reactions were incubated for 20 h at room temperature. (C and D) Identification of platination sites on recombinant FBL by mass spectrometry after incubation with 100 μM oxaliplatin for 16 h. Identified sites were mapped onto disorder prediction of FBL (C) and primary amino acid sequence (D). Gray bars indicate predicted trypsin cleavage sites, black underscores identified peptides, bold red letters modified amino acids or motifs, and bold purple letters RG motifs. (E) Schematic of FBL in vitro phase separation assay. (F) Phase separation of unmodified (0 μM Ox) and oxaliplatin-modified (100 μM Ox, 16 h) FBL-GFP at various concentrations was monitored by measuring turbidity at 430 nm. As a control, 100 μM oxaliplatin was added only immediately before triggering phase separation (100 μM Ox, 0h). Plot markers represent mean values and error bars SD of triplicate measurements. (G) Phase separation propensity of FBL-GFP (at 10 μM) after modification with the indicated amounts of oxaliplatin for 16 h. Phase separation was monitored as in (H). Plot markers represent mean values and error bars SD of triplicate measurements.

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Gel Shift, Recombinant, Western Blot, Incubation, Mass Spectrometry, Sequencing, Modification, In Vitro, Control

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: (A) Cell number versus drug concentration of HT-1080 cells transfected with either GFP, GFP-FBL, or GFP-NPM1, measured 48 h after treatment with the indicated amounts of Pt compounds. Data points represent the mean values from three replicates, error bars the SD, and curves a nonlinear dose-response fit to the data (see ). (B) Comparison of EC 50 values derived from the fits in (B) for oxaliplatin-treated HT-1080 cells rescued with the indicated constructs. Bar heights indicate median values, error bars median deviation and plot markers individual data points. See for statistics. (C) Correlation between expression of the indicated nucleolar protein-coding transcripts (in TPM) and oxaliplatin resistance (quantified by the area under the dose-viability curve, AUC; see ) in colorectal cancers (CRCs; blue) and central nervous system cancers (CNS; purple). Data points denote individual cancer cell lines, orange lines a linear fit to the data, light orange lines the 90% confidence interval of the fit, and ⍴ the Pearson correlation coefficient. See for statistics. (D) Model summarizing the different mechanisms by which oxaliplatin and actinomycin D target nucleolar form and function.

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Concentration Assay, Transfection, Comparison, Derivative Assay, Construct, Expressing

Journal: Cell reports

Article Title: Oxaliplatin disrupts nucleolar function through biophysical disintegration

doi: 10.1016/j.celrep.2022.111629

Figure Lengend Snippet: KEY RESOURCES TABLE

Article Snippet: Oxaliplatin , Acros Organics , AC456131000.

Techniques: Virus, Recombinant, cDNA Synthesis, SYBR Green Assay, Knock-In, Software, Expressing

Journal: Journal of controlled release : official journal of the Controlled Release Society

Article Title: Enhancing anti-tumor immunity through liposomal oxaliplatin and localized immunotherapy via STING activation.

doi: 10.1016/j.jconrel.2023.04.011

Figure Lengend Snippet: Fig. 1. The schematic illustration of liposome-mediated immunochemotherapy. This figure depicts a schematic representation of liposome-mediated immunoche motherapy. The liposomes (OLP) are shown as spherical structures enclosing therapeutic agents such as the chemotherapeutic drug oxaliplatin (OXA) and the STING agonist ADU-S100. The liposomes are designed to target the tumor cells specifically and facilitate the delivery of the therapeutic agents to the TME. Upon reaching the TME, the liposomes are taken up by the tumor cells and the therapeutic agents are released into the surrounding area. The release of OXA triggers the immunogenic cell death of the tumor cells, which further activates the immune system. Meanwhile, the released ADU-S100 activates the STING pathway, promoting the production of type I interferons and cytokines. This results in the recruitment of immune cells such as DCs, which prime T cells for a specific anti-tumor response. The liposome-mediated immunochemotherapy not only enhances the anti-tumor immune response, but also reduces the recruitment of M2 macrophages and reg ulatory T lymphocytes (Tregs) in the TME. These combined effects of liposome-mediated immunochemotherapy result in a more effective and targeted approach for cancer treatment.

Article Snippet: Oxaliplatin was obtained from EDQM (Strasbourg, France).

Techniques: Liposomes

Journal: Journal of controlled release : official journal of the Controlled Release Society

Article Title: Enhancing anti-tumor immunity through liposomal oxaliplatin and localized immunotherapy via STING activation.

doi: 10.1016/j.jconrel.2023.04.011

Figure Lengend Snippet: Fig. 2. The characterization of liposomes. A. TEM (transmission electron microscopy) images of eLP (empty liposomes) and OLP (oxaliplatin-loaded liposomes). B. Size and zeta potential distribution of liposomes. C. In vitro cumulative release behaviors of free oxaliplatin and OLP.

Article Snippet: Oxaliplatin was obtained from EDQM (Strasbourg, France).

Techniques: Liposomes, Transmission Assay, Electron Microscopy, Zeta Potential Analyzer, In Vitro

Journal: Frontiers in Oncology

Article Title: Heme-Dependent ER Stress Apoptosis: A Mechanism for the Selective Toxicity of the Dihydroartemisinin, NSC735847, in Colorectal Cancer Cells

doi: 10.3389/fonc.2020.00965

Figure Lengend Snippet: The combination of NSC735847, 5-Fluorouracil, and folinic acid is more cytotoxic than FOLFOX in human CRC cells. (A,B) HT29 and HCT116 cells were treated for 24 h with vehicle (0.1% DMSO) or different concentrations of (A) NSC735847 (NSC) (1.25, 2.5, 5, 10, and 20 μM) or (B) oxaliplatin (OX) (5, 10, 20, 40, and 80 μM) and the viability of the cells was determined by conducting MTS experiments. (C,D) HT29 and HCT116 cells were treated for 24 h with vehicle or different concentrations of (C) NSC, 5-Fluorouracil (5-FU), and folinic acid (Fol) (FolFNSC) or (D) 5-FU, folinic acid, and oxaliplatin (FOLFOX) and then cell survival was determined by conducting MTS viability assays. (E) HT29 and (F) HCT116 cells were treated for 24 h with 10 μM NSC, 40 μM OXA, FOLFOX (500 μM 5-FU, 100 μM Fol, 40 μM OX), or FolFNSC (500 μM 5-FU, 100 μM Fol, 10 μM NSC) and cell survival was measured by performing MTS viability assays. The data are represented as the mean ± SEM (*indicates a statistically significant difference between the samples and vehicle treated cells, # indicates a statistically significant difference between the samples and FOLFOX treated cells, P < 0.05).

Article Snippet: Oxaliplatin was from LC Laboratories (Woburn, MA).

Techniques: