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non small cell lung cancer cell lines pc 9  (ATCC)


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    Structured Review

    ATCC non small cell lung cancer cell lines pc 9
    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
    Non Small Cell Lung Cancer Cell Lines Pc 9, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 35823 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response"

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    Journal: Biochemistry and Biophysics Reports

    doi: 10.1016/j.bbrep.2026.102568

    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
    Figure Legend Snippet: IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Techniques Used: Concentration Assay, CRISPR

    Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.
    Figure Legend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Techniques Used: Inhibition, Expressing, Control

    Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.
    Figure Legend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Techniques Used: Inhibition



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    ATCC human non small cell lung cancer nsclc cell lines a549
    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    ATCC human non small cell lung cancer a549
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 <t>or</t> <t>PC-9</t> treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.
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    ATCC human non small cell lung cancer a549 cells
    Zotatifin demonstrates dose-dependent inhibition of Mayaro virus (MAYV) replication across multiple cell lines. (A) Chemical structures of rocaglate compounds evaluated in this study. (B) Cell viability assessment in HDFs and HMC3 cells following 24 h treatment with increasing zotatifin concentrations, determined using the MTT assay. (C–H) Antiviral efficacy evaluation across three cell lines. HDFs (C–E) , HMC3 (F–G) , and <t>A549</t> cells (H) were pretreated with rocaglates for 2 h, infected with MAYV strain AVR0565 (MOI = 1). Following 24 h incubation with compounds, viral progeny was quantified by plaque-forming assay. The dashed horizontal line indicates the limit of detection (10 PFU/ml). Data shown for rocaglamide (blue bars), CR-1-31-B (orange bars), and zotatifin (violet bars). (I) Morphological analysis of MAYV-infected HDFs with zotatifin treatment (50 nM). Cells were fixed at 48 h post-infection with a 4% formaldehyde solution and stained with a 2% crystal violet solution. Scale bar: 100 μm. Values represent mean ± standard deviation from three independent experiments, each performed in triplicate (C–H) o quadruplicate (B) . Statistical analysis was performed using a one-way ANOVA, followed by a Dunnett’s post hoc test comparing treated groups to vehicle control. Significance levels: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001.
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    IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: IFN-γ responsiveness correlates DNA damage and repair responses in NSCLC cell lines (A) Relative cell viability of A549 or PC-9 treated with the indicated concentration of IFN-γ for 24 h are shown. Data are presented as mean ± SD. (B) Reactome analysis of the GSE180942 dataset was performed using differential CRISPR β-scores under IFN-γ treatment (Δβ = PC-9 − A549). Bars indicate the normalized enrichment score (NES) for each pathway indicated. Positive NES denotes pathways whose constituent genes are more essential in A549, whereas negative NES denotes pathways more essential in PC-9 upon IFN-γ treatment.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Concentration Assay, CRISPR

    Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: Inhibition of ATM restores NSCLC cells to IFN-γ by inducing DNA damage response (A) Cell viability of A549 (left panel) or PC-9 (right panel) treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05. (B) Expression of γH2AX and b-Actin (loading control) in A549 (left panel) or PC-9 (right panel) cells treated with IFN-γ (1000 ng/ml) and/or KU-55933 (10 μM) for 24 h are shown.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Inhibition, Expressing, Control

    Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Journal: Biochemistry and Biophysics Reports

    Article Title: ATM inhibition restores IFN-γ sensitivity and induces ferroptosis in NSCLC via DNA damage response

    doi: 10.1016/j.bbrep.2026.102568

    Figure Lengend Snippet: Inhibition of ATM in combination with IFN-γ induce ferroptosis in NSCLCs Cell viability of A549 (A) or PC-9 (B) treated with the indicated combination of IFN-γ (1000 ng/ml), KU-55933 (10 μM), Ferrostatin-1 (5 μM), and Liproxstatin-1 (5 μM) for 24 h are shown. Data are presented as mean ± SD. * p < 0.05.

    Article Snippet: The human non-small cell lung cancer cell lines PC-9 (kindly gifted from Dr. Kiura, Okayama University, Japan) and A549 (CCL-185, obtained from American Type Culture Collection) were used.

    Techniques: Inhibition

    Zotatifin demonstrates dose-dependent inhibition of Mayaro virus (MAYV) replication across multiple cell lines. (A) Chemical structures of rocaglate compounds evaluated in this study. (B) Cell viability assessment in HDFs and HMC3 cells following 24 h treatment with increasing zotatifin concentrations, determined using the MTT assay. (C–H) Antiviral efficacy evaluation across three cell lines. HDFs (C–E) , HMC3 (F–G) , and A549 cells (H) were pretreated with rocaglates for 2 h, infected with MAYV strain AVR0565 (MOI = 1). Following 24 h incubation with compounds, viral progeny was quantified by plaque-forming assay. The dashed horizontal line indicates the limit of detection (10 PFU/ml). Data shown for rocaglamide (blue bars), CR-1-31-B (orange bars), and zotatifin (violet bars). (I) Morphological analysis of MAYV-infected HDFs with zotatifin treatment (50 nM). Cells were fixed at 48 h post-infection with a 4% formaldehyde solution and stained with a 2% crystal violet solution. Scale bar: 100 μm. Values represent mean ± standard deviation from three independent experiments, each performed in triplicate (C–H) o quadruplicate (B) . Statistical analysis was performed using a one-way ANOVA, followed by a Dunnett’s post hoc test comparing treated groups to vehicle control. Significance levels: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Broad-spectrum antiviral activity of the synthetic rocaglate zotatifin against Mayaro virus and other viruses

    doi: 10.3389/fcimb.2026.1752166

    Figure Lengend Snippet: Zotatifin demonstrates dose-dependent inhibition of Mayaro virus (MAYV) replication across multiple cell lines. (A) Chemical structures of rocaglate compounds evaluated in this study. (B) Cell viability assessment in HDFs and HMC3 cells following 24 h treatment with increasing zotatifin concentrations, determined using the MTT assay. (C–H) Antiviral efficacy evaluation across three cell lines. HDFs (C–E) , HMC3 (F–G) , and A549 cells (H) were pretreated with rocaglates for 2 h, infected with MAYV strain AVR0565 (MOI = 1). Following 24 h incubation with compounds, viral progeny was quantified by plaque-forming assay. The dashed horizontal line indicates the limit of detection (10 PFU/ml). Data shown for rocaglamide (blue bars), CR-1-31-B (orange bars), and zotatifin (violet bars). (I) Morphological analysis of MAYV-infected HDFs with zotatifin treatment (50 nM). Cells were fixed at 48 h post-infection with a 4% formaldehyde solution and stained with a 2% crystal violet solution. Scale bar: 100 μm. Values represent mean ± standard deviation from three independent experiments, each performed in triplicate (C–H) o quadruplicate (B) . Statistical analysis was performed using a one-way ANOVA, followed by a Dunnett’s post hoc test comparing treated groups to vehicle control. Significance levels: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001.

    Article Snippet: Human dermal fibroblasts (HDFs, Cat. # PCS-201-012), human immortalized microglial cells (HMC3, Cat. # CRL-3304), human non-small cell lung cancer A549 cells (CCL-185), BSC40 (Cat. # CRL-2761), and Vero-E6 cells (CRL-1586) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Inhibition, Virus, MTT Assay, Infection, Incubation, Staining, Standard Deviation, Control

    Zotatifin reduces MAYV E1 and nsP1 protein levels in a dose-dependent manner. HDFs (A) or A549 cells (B) were pretreated with zotatifin at concentrations of 15, 30, and 50 nM for 2 h. Cells were subsequently infected with MAYV strain AVR0565 (MOI = 1) and maintained in the presence of zotatifin throughout the infection period. At 24 h post-infection, viral protein levels were assessed by Western blot analysis using specific antibodies against MAYV E1 and nsP1 proteins. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) served as the loading control. Representative blots from three independent experiments are shown. (C) A549 cells were treated with 50 nM zotatifin or vehicle control and infected with MAYV strain AVR0565. At 24 h post-infection, cells were fixed and processed for immunofluorescence microscopy using antibodies specific for MAYV E1 and nsP1 proteins. Representative immunofluorescence images from at least 10 fields across two independent experiments are presented. Scale bar: 50 μm.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Broad-spectrum antiviral activity of the synthetic rocaglate zotatifin against Mayaro virus and other viruses

    doi: 10.3389/fcimb.2026.1752166

    Figure Lengend Snippet: Zotatifin reduces MAYV E1 and nsP1 protein levels in a dose-dependent manner. HDFs (A) or A549 cells (B) were pretreated with zotatifin at concentrations of 15, 30, and 50 nM for 2 h. Cells were subsequently infected with MAYV strain AVR0565 (MOI = 1) and maintained in the presence of zotatifin throughout the infection period. At 24 h post-infection, viral protein levels were assessed by Western blot analysis using specific antibodies against MAYV E1 and nsP1 proteins. Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) served as the loading control. Representative blots from three independent experiments are shown. (C) A549 cells were treated with 50 nM zotatifin or vehicle control and infected with MAYV strain AVR0565. At 24 h post-infection, cells were fixed and processed for immunofluorescence microscopy using antibodies specific for MAYV E1 and nsP1 proteins. Representative immunofluorescence images from at least 10 fields across two independent experiments are presented. Scale bar: 50 μm.

    Article Snippet: Human dermal fibroblasts (HDFs, Cat. # PCS-201-012), human immortalized microglial cells (HMC3, Cat. # CRL-3304), human non-small cell lung cancer A549 cells (CCL-185), BSC40 (Cat. # CRL-2761), and Vero-E6 cells (CRL-1586) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Infection, Western Blot, Control, Immunofluorescence, Microscopy

    Zotatifin inhibits MAYV replication through stage-specific mechanisms and enhances innate immune responses. (A) Schematic representation of the experimental design for viral cycle analysis, showing the pre-treatment, binding, entry, and post-entry assays protocols. HDFs were treated with zotatifin (50 nM) and infected with MAYV (AVR0565 strain). Viral titers in culture supernatants were quantified by plaque-forming assay for: (B) pre-treatment assay (cells pre-treated with zotatifin before infection), (C) binding assay (zotatifin present during viral adsorption), (D) entry assay (zotatifin added during viral entry phase), and (E) post-entry assay (zotatifin added after viral internalization). (F) Time-of-addition analysis. HDFs were infected with MAYV and zotatifin (50 nM) was added at indicated time points post-infection. Viral titers were determined by plaque-forming assay at 24 h post-infection. The dashed horizontal line indicates the limit of detection (10 PFU/ml). (G–K) Zotatifin upregulates interferon and interferon-stimulated gene expression. A549 and HMC3 cells were treated or untreated with 50 nM zotatifin for 8 h. Relative mRNA expression levels were analyzed by RT-qPCR for: (G) interferon-α ( IFNα ), (H) RIG-I-like receptor ( DDX58 ), (I) myxovirus resistance protein A ( MxA ), (J) interferon-stimulated gene 15 ( ISG15 ), and (K) Toll-like receptor 3 ( TLR3 ). Expression levels were normalized to β-actin using the ΔΔCt method. Data represent mean ± standard deviation from two independent experiments performed in triplicate. Statistical significance was determined by unpaired Student t-test. Significance levels: ns, not significant; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Broad-spectrum antiviral activity of the synthetic rocaglate zotatifin against Mayaro virus and other viruses

    doi: 10.3389/fcimb.2026.1752166

    Figure Lengend Snippet: Zotatifin inhibits MAYV replication through stage-specific mechanisms and enhances innate immune responses. (A) Schematic representation of the experimental design for viral cycle analysis, showing the pre-treatment, binding, entry, and post-entry assays protocols. HDFs were treated with zotatifin (50 nM) and infected with MAYV (AVR0565 strain). Viral titers in culture supernatants were quantified by plaque-forming assay for: (B) pre-treatment assay (cells pre-treated with zotatifin before infection), (C) binding assay (zotatifin present during viral adsorption), (D) entry assay (zotatifin added during viral entry phase), and (E) post-entry assay (zotatifin added after viral internalization). (F) Time-of-addition analysis. HDFs were infected with MAYV and zotatifin (50 nM) was added at indicated time points post-infection. Viral titers were determined by plaque-forming assay at 24 h post-infection. The dashed horizontal line indicates the limit of detection (10 PFU/ml). (G–K) Zotatifin upregulates interferon and interferon-stimulated gene expression. A549 and HMC3 cells were treated or untreated with 50 nM zotatifin for 8 h. Relative mRNA expression levels were analyzed by RT-qPCR for: (G) interferon-α ( IFNα ), (H) RIG-I-like receptor ( DDX58 ), (I) myxovirus resistance protein A ( MxA ), (J) interferon-stimulated gene 15 ( ISG15 ), and (K) Toll-like receptor 3 ( TLR3 ). Expression levels were normalized to β-actin using the ΔΔCt method. Data represent mean ± standard deviation from two independent experiments performed in triplicate. Statistical significance was determined by unpaired Student t-test. Significance levels: ns, not significant; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Article Snippet: Human dermal fibroblasts (HDFs, Cat. # PCS-201-012), human immortalized microglial cells (HMC3, Cat. # CRL-3304), human non-small cell lung cancer A549 cells (CCL-185), BSC40 (Cat. # CRL-2761), and Vero-E6 cells (CRL-1586) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Binding Assay, Infection, Adsorption, Gene Expression, Expressing, Quantitative RT-PCR, Standard Deviation

    Zotatifin inhibits the replication of influenza A, vesicular stomatitis, and vaccinia viruses. A549 cells were pretreated with zotatifin, then infected with PR8-GFP (A–D) , rVSV-GFP (E–G) or vaccinia (H, I) viruses at low (0.5) or high (5) multiplicity of infection (MOI). At 24 h post-infection, the intensity of GFP, and the quantity of viral progeny in PR8-GFP and rVSV-GFP infected cells were assessed using flow cytometry, and a plaque-forming assay. Virus titers in cell lysates of vaccinia virus infected cells were determined by plaque assay. The dashed horizontal line indicates the limit of detection (10 PFU/ml). Data represent mean ± standard deviation from two independent experiments performed in triplicate. Statistical analysis was carried out using a one-way ANOVA followed by a Dunnett’s post hoc test or an unpaired Student t-test. Significance levels: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Broad-spectrum antiviral activity of the synthetic rocaglate zotatifin against Mayaro virus and other viruses

    doi: 10.3389/fcimb.2026.1752166

    Figure Lengend Snippet: Zotatifin inhibits the replication of influenza A, vesicular stomatitis, and vaccinia viruses. A549 cells were pretreated with zotatifin, then infected with PR8-GFP (A–D) , rVSV-GFP (E–G) or vaccinia (H, I) viruses at low (0.5) or high (5) multiplicity of infection (MOI). At 24 h post-infection, the intensity of GFP, and the quantity of viral progeny in PR8-GFP and rVSV-GFP infected cells were assessed using flow cytometry, and a plaque-forming assay. Virus titers in cell lysates of vaccinia virus infected cells were determined by plaque assay. The dashed horizontal line indicates the limit of detection (10 PFU/ml). Data represent mean ± standard deviation from two independent experiments performed in triplicate. Statistical analysis was carried out using a one-way ANOVA followed by a Dunnett’s post hoc test or an unpaired Student t-test. Significance levels: ns, not significant; * p < 0.05; ** p < 0.01; *** p < 0.001; and **** p < 0.0001.

    Article Snippet: Human dermal fibroblasts (HDFs, Cat. # PCS-201-012), human immortalized microglial cells (HMC3, Cat. # CRL-3304), human non-small cell lung cancer A549 cells (CCL-185), BSC40 (Cat. # CRL-2761), and Vero-E6 cells (CRL-1586) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Infection, Flow Cytometry, Virus, Plaque Assay, Standard Deviation

    Zotatifin downregulates the synthesis of viral proteins in influenza A virus, vesicular stomatitis virus, and vaccinia virus infected cells. A549 cells were pretreated with zotatifin, then infected with PR8-GFP (A, B) , rVSV-GFP (C, D) , or vaccinia (E, F) viruses, as previously indicated. At the indicated hours after infection, levels of influenza A NP, VSV G, or vaccinia E3L proteins were evaluated using Western blot analysis. β-actin or GAPDH proteins were used as a loading controls. Representative images from three independent experiments are shown.

    Journal: Frontiers in Cellular and Infection Microbiology

    Article Title: Broad-spectrum antiviral activity of the synthetic rocaglate zotatifin against Mayaro virus and other viruses

    doi: 10.3389/fcimb.2026.1752166

    Figure Lengend Snippet: Zotatifin downregulates the synthesis of viral proteins in influenza A virus, vesicular stomatitis virus, and vaccinia virus infected cells. A549 cells were pretreated with zotatifin, then infected with PR8-GFP (A, B) , rVSV-GFP (C, D) , or vaccinia (E, F) viruses, as previously indicated. At the indicated hours after infection, levels of influenza A NP, VSV G, or vaccinia E3L proteins were evaluated using Western blot analysis. β-actin or GAPDH proteins were used as a loading controls. Representative images from three independent experiments are shown.

    Article Snippet: Human dermal fibroblasts (HDFs, Cat. # PCS-201-012), human immortalized microglial cells (HMC3, Cat. # CRL-3304), human non-small cell lung cancer A549 cells (CCL-185), BSC40 (Cat. # CRL-2761), and Vero-E6 cells (CRL-1586) were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA).

    Techniques: Virus, Infection, Western Blot