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ATCC human ovarian cancer cell line skov3
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 – <t>SKOV3</t> 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.
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ATCC caco 2 cells
HCE suppresses the adhesion and invasion of Salmonella <t>in</t> <t>Caco-2</t> cells. A CCK-8 assay (A) was conducted to evaluate the cytotoxicity of HCE in Caco-2 cells. The effects of HCE on the adhesion (B, D) and invasion (C, E) of ST (B-C) and SP (D-E) to Caco-2 cells were examined at an MOI of 100 (n = 5). Immunofluorescence microscopy was performed to visualize the inhibitory effect of HCE (150 µg/mL) on the invasion of ST (F) and SP (G) in Caco-2 cells. Caco-2 cells infected with the ST Δ invA strain, which was used as a negative control because of its T3SS-1 deficiency showed significantly reduced invasion. ST, Salmonella Typhimurium. SP, Salmonella Pullorum . HCE, Houttuynia cordata extract.
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Evaluation of the protective effects of CG@GelMA on FSN-induced intestinal epithelial barrier disruption in vitro . (A) Immunofluorescence staining of Claudin-1 <t>in</t> <t>Caco-2</t> monolayers under different treatments. Scale bar: 100 μm. (B) Relative fluorescence intensity of Claudin-1. (C) Immunofluorescence staining of Occludin in Caco-2 monolayers. Scale bar: 100 μm. (D) Relative fluorescence intensity of Occludin. (E) Immunofluorescence staining of ZO-1 in Caco-2 monolayers. Scale bar: 100 μm. (F) Relative fluorescence intensity of ZO-1. (G) Schematic diagram of the Caco-2/RAW 264.7 Transwell co-culture system. (H) Relative TEER of Caco-2 cell monolayers after different treatments. (I) Relative fluorescence intensity of FD4 across Caco-2 monolayers under different treatments. Data are presented as means ± SD. Statistical significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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siha  (ATCC)
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Evaluation of the protective effects of CG@GelMA on FSN-induced intestinal epithelial barrier disruption in vitro . (A) Immunofluorescence staining of Claudin-1 <t>in</t> <t>Caco-2</t> monolayers under different treatments. Scale bar: 100 μm. (B) Relative fluorescence intensity of Claudin-1. (C) Immunofluorescence staining of Occludin in Caco-2 monolayers. Scale bar: 100 μm. (D) Relative fluorescence intensity of Occludin. (E) Immunofluorescence staining of ZO-1 in Caco-2 monolayers. Scale bar: 100 μm. (F) Relative fluorescence intensity of ZO-1. (G) Schematic diagram of the Caco-2/RAW 264.7 Transwell co-culture system. (H) Relative TEER of Caco-2 cell monolayers after different treatments. (I) Relative fluorescence intensity of FD4 across Caco-2 monolayers under different treatments. Data are presented as means ± SD. Statistical significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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Evaluation of the protective effects of CG@GelMA on FSN-induced intestinal epithelial barrier disruption in vitro . (A) Immunofluorescence staining of Claudin-1 <t>in</t> <t>Caco-2</t> monolayers under different treatments. Scale bar: 100 μm. (B) Relative fluorescence intensity of Claudin-1. (C) Immunofluorescence staining of Occludin in Caco-2 monolayers. Scale bar: 100 μm. (D) Relative fluorescence intensity of Occludin. (E) Immunofluorescence staining of ZO-1 in Caco-2 monolayers. Scale bar: 100 μm. (F) Relative fluorescence intensity of ZO-1. (G) Schematic diagram of the Caco-2/RAW 264.7 Transwell co-culture system. (H) Relative TEER of Caco-2 cell monolayers after different treatments. (I) Relative fluorescence intensity of FD4 across Caco-2 monolayers under different treatments. Data are presented as means ± SD. Statistical significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.
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FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results <t>obtained</t> <t>from</t> <t>MDA-MB-231</t> one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.
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FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results <t>obtained</t> <t>from</t> <t>MDA-MB-231</t> one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.
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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.

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

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.

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

HCE suppresses the adhesion and invasion of Salmonella in Caco-2 cells. A CCK-8 assay (A) was conducted to evaluate the cytotoxicity of HCE in Caco-2 cells. The effects of HCE on the adhesion (B, D) and invasion (C, E) of ST (B-C) and SP (D-E) to Caco-2 cells were examined at an MOI of 100 (n = 5). Immunofluorescence microscopy was performed to visualize the inhibitory effect of HCE (150 µg/mL) on the invasion of ST (F) and SP (G) in Caco-2 cells. Caco-2 cells infected with the ST Δ invA strain, which was used as a negative control because of its T3SS-1 deficiency showed significantly reduced invasion. ST, Salmonella Typhimurium. SP, Salmonella Pullorum . HCE, Houttuynia cordata extract.

Journal: Poultry Science

Article Title: Houttuynia cordata extract protects against Salmonella infection by targeting type III secretion system 1

doi: 10.1016/j.psj.2026.106937

Figure Lengend Snippet: HCE suppresses the adhesion and invasion of Salmonella in Caco-2 cells. A CCK-8 assay (A) was conducted to evaluate the cytotoxicity of HCE in Caco-2 cells. The effects of HCE on the adhesion (B, D) and invasion (C, E) of ST (B-C) and SP (D-E) to Caco-2 cells were examined at an MOI of 100 (n = 5). Immunofluorescence microscopy was performed to visualize the inhibitory effect of HCE (150 µg/mL) on the invasion of ST (F) and SP (G) in Caco-2 cells. Caco-2 cells infected with the ST Δ invA strain, which was used as a negative control because of its T3SS-1 deficiency showed significantly reduced invasion. ST, Salmonella Typhimurium. SP, Salmonella Pullorum . HCE, Houttuynia cordata extract.

Article Snippet: Caco-2 cells (American Type Culture Collection, ATCC, USA) were cultured in DMEM and seeded into culture plates.

Techniques: CCK-8 Assay, Immunofluorescence, Microscopy, Infection, Negative Control

Evaluation of the protective effects of CG@GelMA on FSN-induced intestinal epithelial barrier disruption in vitro . (A) Immunofluorescence staining of Claudin-1 in Caco-2 monolayers under different treatments. Scale bar: 100 μm. (B) Relative fluorescence intensity of Claudin-1. (C) Immunofluorescence staining of Occludin in Caco-2 monolayers. Scale bar: 100 μm. (D) Relative fluorescence intensity of Occludin. (E) Immunofluorescence staining of ZO-1 in Caco-2 monolayers. Scale bar: 100 μm. (F) Relative fluorescence intensity of ZO-1. (G) Schematic diagram of the Caco-2/RAW 264.7 Transwell co-culture system. (H) Relative TEER of Caco-2 cell monolayers after different treatments. (I) Relative fluorescence intensity of FD4 across Caco-2 monolayers under different treatments. Data are presented as means ± SD. Statistical significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Journal: Bioactive Materials

Article Title: Harnessing the gut–immune–joint axis: Oral microalgae-based thermoresponsive microspheres enhance intra-articular therapy for rheumatoid arthritis

doi: 10.1016/j.bioactmat.2026.01.037

Figure Lengend Snippet: Evaluation of the protective effects of CG@GelMA on FSN-induced intestinal epithelial barrier disruption in vitro . (A) Immunofluorescence staining of Claudin-1 in Caco-2 monolayers under different treatments. Scale bar: 100 μm. (B) Relative fluorescence intensity of Claudin-1. (C) Immunofluorescence staining of Occludin in Caco-2 monolayers. Scale bar: 100 μm. (D) Relative fluorescence intensity of Occludin. (E) Immunofluorescence staining of ZO-1 in Caco-2 monolayers. Scale bar: 100 μm. (F) Relative fluorescence intensity of ZO-1. (G) Schematic diagram of the Caco-2/RAW 264.7 Transwell co-culture system. (H) Relative TEER of Caco-2 cell monolayers after different treatments. (I) Relative fluorescence intensity of FD4 across Caco-2 monolayers under different treatments. Data are presented as means ± SD. Statistical significance: ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: RAW 264.7 macrophages (Procell, Wuhan, China), Caco-2 intestinal epithelial cells (Pricella, Wuhan, China), and IEC-6 small intestinal epithelial cells (ATCC, USA) were maintained in high-glucose DMEM supplemented with 10 % fetal bovine serum (AiTing, Hangzhou, China) and 1 % penicillin-streptomycin (Gibco, USA), with the medium for IEC-6 cells additionally containing 0.1 U/mL human insulin.

Techniques: Disruption, In Vitro, Immunofluorescence, Staining, Fluorescence, Co-Culture Assay

FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results obtained from MDA-MB-231 one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.

Journal: STAR Protocols

Article Title: Protocol for enhancing CRISPR-Cas9 genome editing using histone deacetylase inhibition and engineered virus-like particle delivery

doi: 10.1016/j.xpro.2026.104493

Figure Lengend Snippet: FAME-CRISPR improves CRISPR/Cas9 gene editing efficiency through HDACi mediated chromatin relaxation and precise eVLP delivery (A) shows a brief schematic of the major steps required to improve editing efficacy using FAME-CRISPR workflow. (B), (C), (D), and (E) show representative results obtained from MDA-MB-231 one of the utilized cell lines from the original FAME-CRISPR study ([60nM panobinostat] and [1.5 μM belinostat]) (n = 3 biological replicates for all conditions, and error bars reflect standard deviation). Results and raw data for MDA-MB-231 and other tested cell lines are available in the original study and data availability statement section of STAR Protocols.

Article Snippet: MDA-MB-231 , ATCC , #HTB-26.

Techniques: CRISPR, Standard Deviation