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Image Search Results
Journal: Pharmaceutics
Article Title: Synergistic Encapsulation of Paclitaxel and Sorafenib by Methoxy Poly(Ethylene Glycol)- b -Poly(Caprolactone) Polymeric Micelles for Ovarian Cancer Therapy
doi: 10.3390/pharmaceutics15041206
Figure Lengend Snippet: IC 50 and CI values of paclitaxel (PTX) and sorafenib (SRF) at various molar ratios (n = 3).
Article Snippet:
Techniques:
Journal: Pharmaceutics
Article Title: Synergistic Encapsulation of Paclitaxel and Sorafenib by Methoxy Poly(Ethylene Glycol)- b -Poly(Caprolactone) Polymeric Micelles for Ovarian Cancer Therapy
doi: 10.3390/pharmaceutics15041206
Figure Lengend Snippet: In vitro cytotoxicity analysis of SKOV3-red-fluc ( A ) PTX solution, ( B ) PTX micelle, ( C ) SRF solution, ( D ) SRF micelle, ( E ) PTX/SRF solution, and ( F ) PTX/SRF micelle (n = 6).
Article Snippet:
Techniques: In Vitro
Journal: Pharmaceutics
Article Title: Synergistic Encapsulation of Paclitaxel and Sorafenib by Methoxy Poly(Ethylene Glycol)- b -Poly(Caprolactone) Polymeric Micelles for Ovarian Cancer Therapy
doi: 10.3390/pharmaceutics15041206
Figure Lengend Snippet: Colony formation inhibition in SKOV3-red-fluc cell line solution and micelles ( A ) free PTX, ( B ) PTX micelle, ( C ) free SRF, ( D ) SRF micelle, ( E ) free PTX/SRF, and ( F ) PTX/SRF micelle (n = 3).
Article Snippet:
Techniques: Inhibition
Journal: Pharmaceutics
Article Title: Synergistic Encapsulation of Paclitaxel and Sorafenib by Methoxy Poly(Ethylene Glycol)- b -Poly(Caprolactone) Polymeric Micelles for Ovarian Cancer Therapy
doi: 10.3390/pharmaceutics15041206
Figure Lengend Snippet: ( A ) Morphological observation of tumor spheroids prepared with SKOV3-red-fluc, ( B ) Control, PTX Solution, PTX micelles, PTX/SRF Solution, and PTX/SRF micelles SKOV3-red-fluc tumor spheroid IVIS measured with D-luciferin before treatment and after secondary treatment image (n = 4). ( C ) A graph showing the total luminescence value reflecting the tumor size for the first and second drug treatments based on the tumor spheroid before drug treatment (** p < 0.01, n = 4).
Article Snippet:
Techniques: Control
Journal: Pharmaceutics
Article Title: Synergistic Encapsulation of Paclitaxel and Sorafenib by Methoxy Poly(Ethylene Glycol)- b -Poly(Caprolactone) Polymeric Micelles for Ovarian Cancer Therapy
doi: 10.3390/pharmaceutics15041206
Figure Lengend Snippet: ( A ) Representative IVIS images of an SKOV3-red-fluc cell xenograft model taken 20 days after IV injection with DPBS (control), solution, and micelle, ( B ) relative total flux (% of day 9) value graph of each group (* p < 0.05, n = 5), ( C ) body weight change, ( D ) representative H&E staining of xenograft mouse model.
Article Snippet:
Techniques: IV Injection, Control, Staining
Journal: Oxidative Medicine and Cellular Longevity
Article Title: HSP90AB1 as the Druggable Target of Maggot Extract Reverses Cisplatin Resistance in Ovarian Cancer
doi: 10.1155/2023/9335440
Figure Lengend Snippet: ME enhances the sensitivity of A2780/CDDP and SKOV3/CDDP cells to cisplatin (Cis). Cells were treated with different concentrations of cisplatin with and without ME (6 mg/ml) for 48 h. (a) The viability of A2780 and A2780/CDDP cells was assayed using CCK8 kits. (b) The viability of SKOV3 and SKOV3/CDDP cells was assayed. SKOV3/CDDP cells were infected with lentiviral particles to express luciferase, and then cells were treated with cisplatin (3.2 μ g/ml) and/or ME (4 mg/ml or 6 mg/ml) for 48 h followed by 150 μ g/ml D-luciferin for 10 min. (c) The luciferase-positive SKOV3/CDDP cells were analyzed using Living Image software and a GloMax® 96 Microplate Luminometer. The quantification of luciferase-positive cells is shown on the right. ∗ p ≤ 0.05 vs. blank; # p ≤ 0.05 vs. cisplatin; (d) A2780/CDDP and SKOV3/CDDP cells were double stained with Annexin V-FITC and PI then analyzed using flow cytometry, and the quantitative analysis was located in the right. ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001. (e) Levels of p-p53 in A2780/DDP cells were measured by immunofluorescence staining (400x magnification). The panel under the staining shows the quantitative analysis of p-p53 in A2780/CDDP cells. The nuclei are stained with DAPI. ∗ p ≤ 0.05 vs. blank; # p ≤ 0.05 vs. cisplatin. (f) Representative images of the wound healing assays in A2780/CDDP and SKOV3/CDDP cells are shown, and the panels under the images show the wound closure rate. ∗ p ≤ 0.05 vs. 0 h; # p ≤ 0.05 vs. blank; ns means no significance vs. 0 h. (g) The transwell assay was used to analyze the invasion of A2780 and A2780/CDDP cells. The invasive cell number was quantified using ImageJ and located under the images. ∗ p ≤ 0.05. Three independent experiments were performed with similar results. Data are shown as the mean ± SEM.
Article Snippet: The human
Techniques: Infection, Luciferase, Software, Staining, Flow Cytometry, Immunofluorescence, Transwell Assay
Journal: Oxidative Medicine and Cellular Longevity
Article Title: HSP90AB1 as the Druggable Target of Maggot Extract Reverses Cisplatin Resistance in Ovarian Cancer
doi: 10.1155/2023/9335440
Figure Lengend Snippet: Enrichment analysis of DEGs in A2780/CDDP cells based on high-throughput RNA sequencing. The total RNA from A2780 and A2780/DDP cells was extracted using RNA Miniprep kit reagents. Next-generation sequencing analysis was performed on the BGISEQ-500 platform by BGI Genomic Services. (a) Volcano plot showing significantly upregulated genes (red dots) and downregulated genes (blue dots). (b) A2780 vs. A2780/CDDP Gene Ontology (GO) analysis on a cellular component of DEGs. (c) A2780 vs. A2780/CDDP KEGG pathway enrichment analysis of DEGs. (d) The heat map shows the relative transcript levels of the DEGs in A2780 and A2780/CDDP cells. (e) The protein–protein interaction network shows the upregulated DEGs from A2780/CDDP cells compared with A2780 cells. (f) qRT-PCR analyses of the mRNA levels of MYC in A2780 cells and A2780/CDDP cells. (g) qRT-PCR analyses of the mRNA levels of HSP90AB1 in A2780 cells and A2780/CDDP cells. Three independent experiments were performed with similar results. Data are shown as the mean ± SEM. ∗ p ≤ 0.05, ∗∗∗ p ≤ 0.001.
Article Snippet: The human
Techniques: High Throughput Screening Assay, RNA Sequencing, Next-Generation Sequencing, Quantitative RT-PCR
Journal: Oxidative Medicine and Cellular Longevity
Article Title: HSP90AB1 as the Druggable Target of Maggot Extract Reverses Cisplatin Resistance in Ovarian Cancer
doi: 10.1155/2023/9335440
Figure Lengend Snippet: ME induces cisplatin to promote apoptosis by suppressing the expression of HSP90AB1/IGF1R in cisplatin-resistant ovarian cancer cells. (a) The expression of HSP90AB1, IGF1R, and IGFBP2 in A2780 cells and A2780/CDDP cells was assessed by western blot. (b) The lower panel shows the quantitative analysis. ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001. (c) The expression of HSP90AB1, IGF1R, and IGFBP2 in SKOV3 cells and SKOV3/CDDP cells was assessed by western blot. (d) The lower panel shows the quantitative analysis. ∗ p ≤ 0.05, ∗∗ p ≤ 0.01. The GSH level in A2780 cells (e) and SKOV3 cells (f) was analyzed using a reduced GSH assay kit. ∗ p ≤ 0.05, ns means no significance. Relative mRNA expression of MYC (g), HSP90AB1 (h), and IGF1R (i) in A2780/CDDP cells was determined by real-time PCR. ∗ p ≤ 0.05, ∗∗∗ p ≤ 0.001, ns means no significance. A2780/CDDP and SKOV3/CDDP cells were treated with cisplatin (3.2 μ g/ml) and ME (6 mg/ml) for 48 h. The protein was extracted for further analysis. (j–m) The protein expression of HSP90AB1, IGF1R, MYC, PTEN, p-H2AX, and BCL2 in A2780/CDDP cells (j) and SKOV3/CDDP cells (l) was measured by western blot. The lower panel shows the quantitative analysis of the western blot in A2780/CDDP cells (K) and SKOV3/CDDP cells (m). ∗ p ≤ 0.05, ns means no significance. Drug-resistant cells were treated with cisplatin, ME, or both. The amount of GSH in A2780/CDDP cells (n) and SKOV3/CDDP cells (o) was analyzed using a reduced GSH assay kit. ∗ p ≤ 0.05, ns means no significance. Three independent experiments were performed with similar results. Data are shown as the mean ± SEM.
Article Snippet: The human
Techniques: Expressing, Western Blot, GSH Assay, Real-time Polymerase Chain Reaction
Journal: Oxidative Medicine and Cellular Longevity
Article Title: HSP90AB1 as the Druggable Target of Maggot Extract Reverses Cisplatin Resistance in Ovarian Cancer
doi: 10.1155/2023/9335440
Figure Lengend Snippet: Inhibition of HSP90 ATPase activity with geldanamycin promotes apoptosis and suppresses migration in cisplatin-resistant ovarian cancer cells. A2780/CDDP cells and SKOV3/CDDP cells were pretreated with 5 μ M geldanamycin (In-HSP) for 1 h and then treated with cisplatin (3.2 μ g/ml) and ME (6 mg/ml) for 72 h. (a) A2780/CDDP cells and SKOV3/CDDP cells were double stained with Annexin V-FITC and PI and then analyzed by flow cytometry, and the quantitative analysis was located on the right. ∗ p ≤ 0.05, ∗∗ p ≤ 0.01, ∗∗∗ p ≤ 0.001. (b, c) A2780/CDDP cells and SKOV3/CDDP cells expressing luciferase were pretreated with 150 μ g/ml D-luciferin for 10 min. The luciferase-positive A2780/CDDP cells (b) and SKOV3/CDDP cells (c) were analyzed using Living Image software and a GloMax® 96 Microplate Luminometer. The quantification of luciferase-positive cells is shown on the right. ∗∗∗ p ≤ 0.001, ∗∗∗∗ p ≤ 0.0001. Representative images of the wound healing assays of A2780/CDDP cells (d) and SKOV3/CDDP cells (e) are shown, and the quantification of the wound closure rate is on the right. ∗ p ≤ 0.05 vs. 0 h; ns mean no significance vs. 0 h; ## p ≤ 0.01. (f) The expression of HSP90AB1, IGF1R, p-H2AX, p-p53, and BAX in A2780/CDDP cells was analyzed by western blot. (g) The panel on the right shows the quantitative analysis. ∗ p ≤ 0.05. (h) The expression of HSP90AB1, IGF1R, p-H2AX, p-p53, and BCL2 in SKOV3/CDDP cells was measured by western blot. (i) The panel on the right shows the quantitative analysis. ∗ p ≤ 0.05. (j–m) The coimmunoprecipitation assay. SKOV3/CDDP cells were treated with geldanamycin for 24 h. The expression levels of HSP90AB1 and IGF1R were measured (j), and the panel on the right shows the quantitative analysis (k). ∗ p ≤ 0.05. The same cell lysates were immunoprecipitated with IGF1R, HSP90AB1, and isoform-matched immunoglobulin (IgG). (l) Western blot assays of SKOV3/CDDP cells using site-specific antibodies against HSP90AB1 and IGF1R, and the panel on the right shows the quantitative analysis (m). ∗ p ≤ 0.05. Three independent experiments were performed with similar results. Data are shown as the mean ± SEM.
Article Snippet: The human
Techniques: Inhibition, Activity Assay, Migration, Staining, Flow Cytometry, Expressing, Luciferase, Software, Western Blot, Co-Immunoprecipitation Assay, Immunoprecipitation
Journal: American Journal of Cancer Research
Article Title: Overexpression of MEF2D contributes to oncogenic malignancy and chemotherapeutic resistance in ovarian carcinoma
doi:
Figure Lengend Snippet: Analyses of MEF2D expression in OC cell lines and patient samples. A. Data on MEF2D DNA copy number and mRNA expression in ovarian cancer and normal ovarian tissue from several study groups deposited in the Oncomine database (www.oncomine.org). B. The protein expression of MEF2D in normal human ovarian epithelial cells (IOSE) and human OC cells (OVCAR3, SKOV3) was determined by western blot assays. C. The protein expression of MEF2D in normal ovarian tissues (N1-N4) and human OC tissues (T1-T12) was determined by western blot assays. Error bars represent the s.d. of triplicate measurements. *P < 0.05; **P < 0.01; ***P < 0.001. D. IHC analysis of MEF2D protein expression in normal ovarian tissues, and OC tissues Original magnifications: × 200 and × 400. E. IHC analysis of IKBKE and HPSE protein expression in normal ovarian tissues, and OC tissues Original magnifications: × 200 and × 400.
Article Snippet: Cell lines culture and establishment of
Techniques: Expressing, Western Blot
Journal: American Journal of Cancer Research
Article Title: Overexpression of MEF2D contributes to oncogenic malignancy and chemotherapeutic resistance in ovarian carcinoma
doi:
Figure Lengend Snippet: Effect of MEF2D knockdown on proliferation and apoptosis of OC cells in vitro. A. CCK-8 assays were performed to determine the effects of MEF2D knockdown on the proliferation of SKOV3 and OVCAR3 cells. Cell viability was determined at 0, 12, 24, 48 and 72 h. B. Flowcytometry assays were performed to determine the effects of MEF2D knockdown on the apoptosis of SKOV3 and OVCAR3 cells. C. Effects of MEF2D knockdown on proliferation-associated protein cyclin-D1 and c-myc and apoptosis-related protein caspase3 and cleaved caspase3 were analyzed by western blotting in SKOV3 and OVCAR3 cells. Error bars represent the s.d. of triplicate measurements. *P < 0.05; **P < 0.01; ***P < 0.001.
Article Snippet: Cell lines culture and establishment of
Techniques: Knockdown, In Vitro, CCK-8 Assay, Western Blot
Journal: American Journal of Cancer Research
Article Title: Overexpression of MEF2D contributes to oncogenic malignancy and chemotherapeutic resistance in ovarian carcinoma
doi:
Figure Lengend Snippet: Effect of MEF2D knockdown on invasion and migration of OC cells in vitro. A. The migration abilities of SKOV3 and OVCAR3 were measured through testing the wound closure after MEF2D knockdown using wound healing assays. B. Transwell assays were used to detect the migration and invasion abilities after MEF2D knockdown in SKOV3 and OVCAR3 cells. Original magnifications, × 200 and × 400. C. Effects of MEF2D knockdown on migration associated protein MMP9 were analyzed by western blotting in SKOV3 and OVCAR3 cells. Error bars represent the s.d. of triplicate measurements. *P < 0.05; **P < 0.01; ***P < 0.001.
Article Snippet: Cell lines culture and establishment of
Techniques: Knockdown, Migration, In Vitro, Western Blot
Journal: American Journal of Cancer Research
Article Title: Overexpression of MEF2D contributes to oncogenic malignancy and chemotherapeutic resistance in ovarian carcinoma
doi:
Figure Lengend Snippet: Effect of MEF2D knockdown on tumorigenecity of ovarian carcinoma cells in vivo. A, B. OVCAR3 cells were subcutaneously inoculated in SCID mice, which were randomly grouped to NC or siMEF2D001 (n = 6 for each group) and then injected with NC or siMEF2D001 every 3 days. 28 days later tumors were removed for analysis. Each tumor formed was volumed and weighted. The weight and volume of established tumors was measured and is shown in a scatter plot. C. Immunohistochemical analysis of MEF2D expression was performed on OVCAR3 tumor xenografts. The representative images are shown (with original magnification, of × 200 and × 400).
Article Snippet: Cell lines culture and establishment of
Techniques: Knockdown, In Vivo, Injection, Immunohistochemical staining, Expressing