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bj normal human foreskin primary fibroblast cell line  (ATCC)


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    Structured Review

    ATCC bj normal human foreskin primary fibroblast cell line
    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), <t>fibroblast</t> proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
    Bj Normal Human Foreskin Primary Fibroblast Cell Line, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1825 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bj normal human foreskin primary fibroblast cell line/product/ATCC
    Average 99 stars, based on 1825 article reviews
    bj normal human foreskin primary fibroblast cell line - by Bioz Stars, 2026-03
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    Images

    1) Product Images from "Chitosan-dextran sulfate nanocapsules for enhanced tigecycline efficacy against non-typhoidal Salmonella enterica"

    Article Title: Chitosan-dextran sulfate nanocapsules for enhanced tigecycline efficacy against non-typhoidal Salmonella enterica

    Journal: Scientific Reports

    doi: 10.1038/s41598-026-35229-7

    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
    Figure Legend Snippet: TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.

    Techniques Used: Infection, Staining, Control



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    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), <t>fibroblast</t> proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
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    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), <t>fibroblast</t> proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
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    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), <t>fibroblast</t> proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
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    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), <t>fibroblast</t> proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.
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    Image Search Results


    TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.

    Journal: Scientific Reports

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    Figure Lengend Snippet: TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.

    Article Snippet: BJ normal human foreskin primary fibroblast cell line (ATCC CRL-2522) was used for studying safety of CD-TGC nanocapsules.

    Techniques: Infection, Staining, Control

    Cell compatibility of CoPc‐Lig NPs. A) Cell viability of fibroblasts (black bars) and keratinocytes (white bars) exposed to different concentrations of CoPc‐Lig NPs for 24 h. B) Confocal images showing cell internalization of CoPc‐Lig NPs (0.5 mg/mL) by fibroblasts and keratinocytes. The dark areas in brightfield images represent CoPc‐Lig NPs, while the fluorescence channels show cell nuclei (Blue), and cell cytoskeleton (green).

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    doi: 10.1002/mabi.202500532

    Figure Lengend Snippet: Cell compatibility of CoPc‐Lig NPs. A) Cell viability of fibroblasts (black bars) and keratinocytes (white bars) exposed to different concentrations of CoPc‐Lig NPs for 24 h. B) Confocal images showing cell internalization of CoPc‐Lig NPs (0.5 mg/mL) by fibroblasts and keratinocytes. The dark areas in brightfield images represent CoPc‐Lig NPs, while the fluorescence channels show cell nuclei (Blue), and cell cytoskeleton (green).

    Article Snippet: Bacterial strains ( Staphylococcus aureus ATCC 6538 and Pseudomonas aeruginosa ATCC 9027) and human fibroblast cell line (ATCC‐SCRC‐1041, HFF‐1) were purchased from the American Type Culture Collection (ATCC LGC Standards, Italy).

    Techniques: Fluorescence

    BJ-5ta cells were transfected with either a non-specific control siRNA (siC) or an eIF5B-specific siRNA pool (si-eIF5B). (A) Following 24 h of transfection, cells were treated with either vehicle control or TRAIL (100 ng/mL). Cell viability was assessed after an additional 72 h using alamarBlue TM assays. (B) Annexin V and 7-AAD staining and flow cytometric analysis of transfected cells. The top two panels, siC and siC + TRAIL, the bottom two panels, si5B and si5B + TRAIL, were harvested at 96 h post-transfection and treated with Annexin V + 7AAD. Contour plots are divided into quadrants Live (lower left; cells staining negative for both 7-AAD and annexin V), Q1 (upper left; cells staining positive for 7-AAD but negative for annexin V), Early apoptosis (lower right; staining annexin V positive and 7-AAD negative), and Late apoptosis (upper right; staining positive for both 7-AAD and annexin V). (C) Representative immunoblots probing for eIF5B, XIAP, Bcl-xL, cIAP1, cFLIPs, DR 4, DR 5, and β-actin (internal control) are shown. ( D) Control and eIF5B-depleted BJ-5ta cells were treated with the 4EGI-1 inhibitor to inhibit cap-dependent translation. Levels of XIAP were monitored under control and the 4EGI-1 treatment conditions. (E) eIF5B-bound RNA immunoprecipitations (RIPs) followed by qRT-PCR measurements of input-normalized tRNAiMet levels from BJ-5ta vs UMSCC-29. Data are presented as mean ± SEM from three independent biological replicates, with statistical significance indicated as follows: *, p < 0.05; **, p < 0.01; ***, p < 0.001.

    Journal: bioRxiv

    Article Title: Eukaryotic Initiation Factor 5B (eIF5B)-Driven Translational Control Impacts Oral Squamous Cell Carcinoma Pathophysiology

    doi: 10.64898/2026.01.30.702967

    Figure Lengend Snippet: BJ-5ta cells were transfected with either a non-specific control siRNA (siC) or an eIF5B-specific siRNA pool (si-eIF5B). (A) Following 24 h of transfection, cells were treated with either vehicle control or TRAIL (100 ng/mL). Cell viability was assessed after an additional 72 h using alamarBlue TM assays. (B) Annexin V and 7-AAD staining and flow cytometric analysis of transfected cells. The top two panels, siC and siC + TRAIL, the bottom two panels, si5B and si5B + TRAIL, were harvested at 96 h post-transfection and treated with Annexin V + 7AAD. Contour plots are divided into quadrants Live (lower left; cells staining negative for both 7-AAD and annexin V), Q1 (upper left; cells staining positive for 7-AAD but negative for annexin V), Early apoptosis (lower right; staining annexin V positive and 7-AAD negative), and Late apoptosis (upper right; staining positive for both 7-AAD and annexin V). (C) Representative immunoblots probing for eIF5B, XIAP, Bcl-xL, cIAP1, cFLIPs, DR 4, DR 5, and β-actin (internal control) are shown. ( D) Control and eIF5B-depleted BJ-5ta cells were treated with the 4EGI-1 inhibitor to inhibit cap-dependent translation. Levels of XIAP were monitored under control and the 4EGI-1 treatment conditions. (E) eIF5B-bound RNA immunoprecipitations (RIPs) followed by qRT-PCR measurements of input-normalized tRNAiMet levels from BJ-5ta vs UMSCC-29. Data are presented as mean ± SEM from three independent biological replicates, with statistical significance indicated as follows: *, p < 0.05; **, p < 0.01; ***, p < 0.001.

    Article Snippet: CAL-33 and BJ-5ta (immortalized fibroblast) cell lines were obtained from American Type Culture Collection (ATCC; Virginia, USA), and UMSCC-1 and UMSCC-29 were obtained from the University of Michigan (Michigan, USA).

    Techniques: Transfection, Control, Staining, Western Blot, Quantitative RT-PCR

    BrdU incorporation assay was used to measure cell proliferation. Quantification shows the percentage of BrdU-labeled cells in control (siC) and si5B-treated groups. Data are presented as mean ± SEM; ***p < 0.001. (A) UMSCC-29 (B) BJ-5ta (C) Collagen-based invasion assay was used to evaluate cell invasiveness in control (siC) and si5B-treated groups. Cells were seeded onto collagen matrices and allowed to invade for a defined period (48-72 hours). The number of invading cells was quantified and expressed as the mean ± SEM. Microscopy images of invading cells (C; left panel) , quantification (C; right panel) . Phase contrast microscopy images showing wound area in siC/si5B-treated OSCC cells at the time of scratch introduction (T = 0 h) & at T = 30 h wound closure (c; top panel) . Quantification of the percentage of wound area covered after 30 hours, normalized to wound area at the time of scratch introduction (c; lower panel) . (E) Representative images of the endothelial HUVEC cells tube formation assay treated with conditioned media from siC- or si5B-transfected OSCC. ImageJ angiogenesis macro software quantified Junctions, segments, and nodes. OSCC cells were transfected with either control siRNA (siC) or eIF5B-specific siRNA (si5B) and incubated for 96 hours. (F) The conditioned media for the control and eIF5B-depleted OSCC cells were analyzed for angiogenic biomarkers (lower panel) using EVE Technologies. (G) Representative images of immunoblots quantified probing for eIF5B, p-EGFR, EGFR, p-ERK, ERK, p-NF-kB, NF-kB, HIF1α, VEGFA, and β-actin (internal control). Data are presented as mean ± SEM from three independent biological replicates, with statistical significance indicated as follows: *, p < 0.05; **, p < 0.01; ***, p < 0.001, and ****, p< 0.0001.

    Journal: bioRxiv

    Article Title: Eukaryotic Initiation Factor 5B (eIF5B)-Driven Translational Control Impacts Oral Squamous Cell Carcinoma Pathophysiology

    doi: 10.64898/2026.01.30.702967

    Figure Lengend Snippet: BrdU incorporation assay was used to measure cell proliferation. Quantification shows the percentage of BrdU-labeled cells in control (siC) and si5B-treated groups. Data are presented as mean ± SEM; ***p < 0.001. (A) UMSCC-29 (B) BJ-5ta (C) Collagen-based invasion assay was used to evaluate cell invasiveness in control (siC) and si5B-treated groups. Cells were seeded onto collagen matrices and allowed to invade for a defined period (48-72 hours). The number of invading cells was quantified and expressed as the mean ± SEM. Microscopy images of invading cells (C; left panel) , quantification (C; right panel) . Phase contrast microscopy images showing wound area in siC/si5B-treated OSCC cells at the time of scratch introduction (T = 0 h) & at T = 30 h wound closure (c; top panel) . Quantification of the percentage of wound area covered after 30 hours, normalized to wound area at the time of scratch introduction (c; lower panel) . (E) Representative images of the endothelial HUVEC cells tube formation assay treated with conditioned media from siC- or si5B-transfected OSCC. ImageJ angiogenesis macro software quantified Junctions, segments, and nodes. OSCC cells were transfected with either control siRNA (siC) or eIF5B-specific siRNA (si5B) and incubated for 96 hours. (F) The conditioned media for the control and eIF5B-depleted OSCC cells were analyzed for angiogenic biomarkers (lower panel) using EVE Technologies. (G) Representative images of immunoblots quantified probing for eIF5B, p-EGFR, EGFR, p-ERK, ERK, p-NF-kB, NF-kB, HIF1α, VEGFA, and β-actin (internal control). Data are presented as mean ± SEM from three independent biological replicates, with statistical significance indicated as follows: *, p < 0.05; **, p < 0.01; ***, p < 0.001, and ****, p< 0.0001.

    Article Snippet: CAL-33 and BJ-5ta (immortalized fibroblast) cell lines were obtained from American Type Culture Collection (ATCC; Virginia, USA), and UMSCC-1 and UMSCC-29 were obtained from the University of Michigan (Michigan, USA).

    Techniques: BrdU Incorporation Assay, Labeling, Control, Invasion Assay, Microscopy, Tube Formation Assay, Transfection, Software, Incubation, Western Blot

    BJ-5ta cells were transfected with either control siRNA (siC) or eIF5B-specific siRNA (si5B) and incubated for 96 hours. TRAIL (100 ng/mL) treatment was performed for 4 hours, then the media was collected. The conditioned media for the control and eIF5B-depleted BT5Ta cells were analyzed for angiogenic biomarkers using EVE Technologies. The level of distinct angiogenic biomarkers was decreased in the spent media of eIF5B-depleted BJ-5ta cells. Data are expressed as mean ± SEM for three biological replicates. Statistical significance is indicated as *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.

    Journal: bioRxiv

    Article Title: Eukaryotic Initiation Factor 5B (eIF5B)-Driven Translational Control Impacts Oral Squamous Cell Carcinoma Pathophysiology

    doi: 10.64898/2026.01.30.702967

    Figure Lengend Snippet: BJ-5ta cells were transfected with either control siRNA (siC) or eIF5B-specific siRNA (si5B) and incubated for 96 hours. TRAIL (100 ng/mL) treatment was performed for 4 hours, then the media was collected. The conditioned media for the control and eIF5B-depleted BT5Ta cells were analyzed for angiogenic biomarkers using EVE Technologies. The level of distinct angiogenic biomarkers was decreased in the spent media of eIF5B-depleted BJ-5ta cells. Data are expressed as mean ± SEM for three biological replicates. Statistical significance is indicated as *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001.

    Article Snippet: CAL-33 and BJ-5ta (immortalized fibroblast) cell lines were obtained from American Type Culture Collection (ATCC; Virginia, USA), and UMSCC-1 and UMSCC-29 were obtained from the University of Michigan (Michigan, USA).

    Techniques: Transfection, Control, Incubation

    The cytotoxic effects of SP09 on NSCLC cell lines and normal lung cells at 72 h. (a) MTT assay showed the cell viability of three EGFR -mutant and KRAS -mutant NSCLC cell lines (H1975, PC9, H1650, A549, H460, and H358), human normal lung epithelial cells (BEAS-2B) and human lung fibroblast cells (CCD19) treated with SP09 for 72 h, all data presented as mean ± SD ( n = 3), **** P < 0.0001, ** P < 0.01, * P < 0.05.

    Journal: Anti-Cancer Drugs

    Article Title: A novel anticancer natural product SP09 selectively targets KRAS-mutant NSCLC through LKB1/AMPK/mTOR modulation: implications for novel therapeutic development

    doi: 10.1097/CAD.0000000000001773

    Figure Lengend Snippet: The cytotoxic effects of SP09 on NSCLC cell lines and normal lung cells at 72 h. (a) MTT assay showed the cell viability of three EGFR -mutant and KRAS -mutant NSCLC cell lines (H1975, PC9, H1650, A549, H460, and H358), human normal lung epithelial cells (BEAS-2B) and human lung fibroblast cells (CCD19) treated with SP09 for 72 h, all data presented as mean ± SD ( n = 3), **** P < 0.0001, ** P < 0.01, * P < 0.05.

    Article Snippet: Human NSCLC cell lines A549 and H460 ( KRAS G12C mutation), PC9 ( EGFR delE746-A750 mutation), and the normal lung fibroblast cell lines CCD19 and BEAS-2B were obtained from the American Type Culture Collection (ATCC, Manassas, Virginia, USA).

    Techniques: MTT Assay, Mutagenesis