Journal: Genes & Diseases

Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

doi: 10.1016/j.gendis.2025.101978

Figure Lengend Snippet: Specific IFN-γ and TNF-α release of T lymphocytes transduced with TIM-3-silenced HER2-specific chimeric antigen receptor (CAR) or HER2-specific CAR. (A, B) TIM-3-silenced CAR-T cells and control T cells were co-incubated with Galectin-9 + or Galectin-9 – SKOV3 tumor cells (E:T ratio 5:1 or 10:1). At 20 h after coculture, a specific enzyme-linked immunosorbent assay was used to analyze the supernatant for IFN-γ cytokine-release. Results were presented as mean ± standard deviation. (C, D) The detection of TNF-α in the same culture supernatant. Results were presented as mean ± standard deviation. ∗ P < 0.05 and ∗∗ P < 0.01.

Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

Techniques: Transduction, Control, Incubation, Enzyme-linked Immunosorbent Assay, Standard Deviation

Journal: Genes & Diseases

Article Title: Blockade of co-inhibitory receptor immune checkpoint protein TIM3/CD366 augments the anti-cancer activity of CAR-T therapy in solid tumors: An ovarian cancer example

doi: 10.1016/j.gendis.2025.101978

Figure Lengend Snippet: TIM-3 silencing augmented the anti-tumor activity of chimeric antigen receptor-T (CAR-T) cells in vivo . 2 × 10 6 SKOV3 tumor cells expressing luciferase were intraperitoneally inoculated in a xenograft mouse model, and 7 days after inoculation, the 2 × 10 6 HER2-specific CAR-T kdTim-3 cells or CAR-T cells, or untreated T cells were intraperitoneally administered. (A, B) Tumor growth was monitored using an in vivo imaging system. (C) Survival curve of 80-day post-treatment. ∗ P < 0.05 and ∗∗ P < 0.01.

Article Snippet: Human cervical cancer cell line HeLa, lentivirus packaging cell line HEK 293TD, and human ovarian cancer cell line SKOV3 were purchased from American Type Culture Collection (Manassas, Virginia, USA) and cultured in Dulbecco's modified Eagle's medium (Invitrogen, Grand Island, New York) supplemented with 10% heat-inactivated fetal bovine serum.

Techniques: Activity Assay, In Vivo, Expressing, Luciferase, In Vivo Imaging

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin dose‐dependently decreases the growth of ovarian cancer cells. The ovarian cancer cell lines, OVCAR‐3 and SKOV‐3, were treated with PCG (from 6.25 to 200 µM) for 24, 48, and 72 h. Cell proliferation was detected by the WST assay. PCG caused a decrease in the growth of (A–C) OVCAR 3 cells and (D–F) SKOV‐3 cells with varying IC 50 s. IC 50 dose concentrations are presented in (G–I) for OVCAR‐3 cells and (J–L) SKOV‐3 cells. Following the statistical analysis, the data in the graphs have been derived from at least three repeated experiments and shown as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: WST Assay, Derivative Assay, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin suppressed the colony formation ability of ovarian cancer cells. The ovarian cancer cell lines, OVCAR‐3 and SKOV‐3, were treated with PCG (from 6.25 to 200 µM) for 48 h and then incubated for 14 days. PCG causes a decrease in the colony formation ability of the (A) OVCAR‐3 and (B) SKOV‐3 cells. The inhibitory effect was more prominent in the OVCAR‐3 as compared to SKOV‐3 cells.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Incubation

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin decreased the migration ability of ovarian cancer cells. The wound healing assay showed a decrease in the ability of ovarian cancer cells to migrate after PCG treatment. PCG caused such an effect in 48 h in (A) OVCAR‐3 cells and for 24 and 48 h in (B) SKOV‐3 cells. The highest cell migration inhibitory effects were obtained in the SKOV‐3 cells as compared to OVCAR‐3 cells. Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Migration, Wound Healing Assay, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin suppressed the transwell migration ability of ovarian cancer cells. To assess the transwell migration ability of PCG on the ovarian cancer cells, the OVCAR‐3 and SKOV‐3 were subjected to 48 h to PCG at various doses (50, 100, and 200 µM). PCG treatment resulted in the decreased transwell migration ability of the (A) OCAR‐3 and (B) SKOV‐3 cells. (C) Western blot assay revealed a decrease in the N‐cadherin, while an increase in E‐cadherin was observed in SKOV‐3 cancer cells. Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Migration, Western Blot, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin disrupted the mitochondrial membrane potential in ovarian cancer cells. Representative images for the analysis of MMP through the JC‐10 assay in (A) OVCAR‐3 cells and (B) SKOV‐3 cells. All cells were seeded at a density of 4 × 10 3 per well in cell culture dishes and treated with (0.1% DMSO) and PCG (50, 100, and 200 µM). Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Membrane, Cell Culture, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin caused an increase in ROS production in ovarian cancer cells. For the quantification of the ROS, the ovarian cancer cells were subjected to PCG for 48 h before employing the MitoSOX assay. There was an increase in the ROS generation at higher doses for (A) OVCAR‐3 and (B) SKOV‐3 cells. Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Mitosox Assay, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin caused apoptosis in ovarian cancer cells. Representative images for the analysis of Annexin V/PI assay in (A) OVCAR‐3 and (B) SKOV‐3 cells. All cells were seeded at a density of 8 × 10 4 per well in cell culture dishes and treated with (0.1% DMSO) and PCG (50, 100, and 200 µM). (C) Representative image of the BAX expression in the SKOV‐3 cells. Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Cell Culture, Expressing, Control

Journal: Journal of Biochemical and Molecular Toxicology

Article Title: Punicalagin Inhibits the Growth and Proliferation of Ovarian Epithelial Adenocarcinoma Cells Via Apoptosis and Autophagic Cell Death

doi: 10.1002/jbt.70908

Figure Lengend Snippet: Punicalagin causes autophagy in ovarian cancer cells. Representative images for the analysis of autophagy through Acridine Orange staining in (A) OVCAR‐3 and (B) SKOV‐3 cells. All cells were seeded at a density of 4 × 10 3 per well in cell culture dishes and treated with (0.1% DMSO) and PCG (50, 100, and 200 µM). Punicalagin caused autophagy in the OVCAR‐3 cell line. (C) Representative image of the BAX expression in the OVCAR‐3 cells. Data were obtained after statistical analysis using at least three repeated experiments, presented in graphs as the mean ± SD. * p ≤ 0.05 compared to control.

Article Snippet: Ovarian cancer cell lines SKOV‐3 and OVCAR‐3 were obtained from ATCC (Manassas, USA).

Techniques: Staining, Cell Culture, Expressing, Control

Journal: bioRxiv

Article Title: Modular Albumin-Chaperoned NIR-II Nanofluorophores Enables Pan-Ovarian Cancer Imaging Across Multiscale Tumor Models

doi: 10.64898/2026.05.06.717945

Figure Lengend Snippet: (a) RNA sequencing data confirming the biomarker expression levels of FOLR1 and SPARC genes in SKOV3 and OVCAR8 tumor cells. (b) SKOV3 cell viability following BSA-FA@SP2 treatment [1-200µg/mL]. (c) IVIS fluorescence images of SKOV3 cultures after 24h treatment with DSPE-PEG@, BSA@, and BSA-FA@SP2 nanofluorophores, with (d) corresponding radiant intensities. (e) Schematic diagram showing experimental designs for time-dependent uptake studies. (f,h) IVIS fluorescence images of cellular uptake of BSA-FA@SP2 in (f) SKOV3 and (h) OVCAR8, with (g,i) corresponding radiant intensities. (j) Schematic diagram showing experimental designs for inhibition studies. (k, m) IVIS fluorescence images of cell uptake of BSA-FA@SP2 in (k) SKOV3 and (m) OVCAR8 following treatment with media (control: microcentrifuge tube 2), SPARC-blocking solution (10µM, microcentrifuge tube 3), and FOLR-blocking solution (10µM, microcentrifuge tube 4). microcentrifuge tube 1 serves as a cell media control, with (l,n) corresponding radiant intensities. All IVIS images were collected with λ ex : 675nm and λ em : 840nm.

Article Snippet: Tumor-On-Chip Cell Cluster Growth and Cell Viability: The human ovarian carcinoma cell line SKOV3 (ATCC) was maintained and expanded following standard culture protocols as previously described.

Techniques: RNA Sequencing, Biomarker Discovery, Expressing, Fluorescence, Inhibition, Control, Blocking Assay

Journal: bioRxiv

Article Title: Modular Albumin-Chaperoned NIR-II Nanofluorophores Enables Pan-Ovarian Cancer Imaging Across Multiscale Tumor Models

doi: 10.64898/2026.05.06.717945

Figure Lengend Snippet: (a) Schematic of the on-chip platform featuring a microfluidic channel mimicking leaky vasculature and a tumor cluster. (b) Representative bright-field (top) and live/dead fluorescence (bottom) images of SKOV3 cell clusters. (c) Live/dead assay fluorescence images of SKOV3 clusters following 36h perfusion of nanofluorophore treatments with (d) corresponding cell viability quantification using a MATLAB script (See Experimental Methods), n = 6. (e-g) IVIS images of SKOV3 clusters after 36h perfusion with (e) DSPE-PEG@SP2, (f) BSA@SP2, and (g) BSA-FA@SP2 with (h) respective radiant intensities, n = 6. All IVIS images were collected with λ ex : 675nm and λ em : 840nm.

Article Snippet: Tumor-On-Chip Cell Cluster Growth and Cell Viability: The human ovarian carcinoma cell line SKOV3 (ATCC) was maintained and expanded following standard culture protocols as previously described.

Techniques: Fluorescence, Live Dead Assay