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ATCC human epithelial cells
Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
Human Epithelial Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Croda International Plc dopc powder
Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of <t>PC3</t> cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.
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ATCC mature human lymphocytes
Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of <t>PC3</t> cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.
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ATCC human epidermal melanocytes
STAT1 and TUBB4A expression levels are significantly correlated and upregulated in melanoma. (A) Analysis of data in the Gene Expression Profiling Interactive Analysis 2 database revealed a significant elevation of STAT1 expression in melanoma tissues. Quantification of (B) STAT1 and (C) TUBB4A mRNA levels in 31 paired melanoma and normal tissue samples from patients with SKCM demonstrated a significant upregulation of both STAT1 and TUBB4A expression in melanoma tissues. (D) Correlation analysis of STAT1 and TUBB4A mRNA levels in melanoma samples showed a significant positive correlation. Comparative analysis of (E) STAT1 and (F) TUBB4A mRNA expression in normal HEM and melanoma cell lines revealed significantly higher expression in the melanoma cell lines. *P<0.05 between groups; **P<0.01 compared with HEM cells. HEM, human epidermal <t>melanocytes;</t> STAT1, signal transducer and activator of transcription 1; TUBB4A, tubulin β4A; TPM, transcripts per million; SKCM, skin cutaneous melanoma.
Human Epidermal Melanocytes, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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ATCC primary peripheral blood mononuclear cells (pbmc), normal, human
STAT1 and TUBB4A expression levels are significantly correlated and upregulated in melanoma. (A) Analysis of data in the Gene Expression Profiling Interactive Analysis 2 database revealed a significant elevation of STAT1 expression in melanoma tissues. Quantification of (B) STAT1 and (C) TUBB4A mRNA levels in 31 paired melanoma and normal tissue samples from patients with SKCM demonstrated a significant upregulation of both STAT1 and TUBB4A expression in melanoma tissues. (D) Correlation analysis of STAT1 and TUBB4A mRNA levels in melanoma samples showed a significant positive correlation. Comparative analysis of (E) STAT1 and (F) TUBB4A mRNA expression in normal HEM and melanoma cell lines revealed significantly higher expression in the melanoma cell lines. *P<0.05 between groups; **P<0.01 compared with HEM cells. HEM, human epidermal <t>melanocytes;</t> STAT1, signal transducer and activator of transcription 1; TUBB4A, tubulin β4A; TPM, transcripts per million; SKCM, skin cutaneous melanoma.
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Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Journal: The Cell Surface

Article Title: Compromising UPD-sugar nucleotide biosynthesis attenuates Candida albicans viability, virulence and drug sensitivity

doi: 10.1016/j.tcsw.2026.100170

Figure Lengend Snippet: Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

Article Snippet: Human epithelial cells derived from a vulvar squamous cell carcinoma (A-431 cell line; ATCC No.: CRL-1555) were cultured and maintained in DMEM medium supplemented with 10% ( v /v) heat inactivated foetal calf serum, 5% penicillin and 5% streptomycin.

Techniques: Lactate Dehydrogenase Assay, Incubation, Activity Assay, Control, Infection, Injection

Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Journal: Journal of Bone Oncology

Article Title: Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype

doi: 10.1016/j.jbo.2026.100754

Figure Lengend Snippet: Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Article Snippet: PC3 prostate tumour cells (ATCC CRL-1435), 4T1 breast tumour cells (CRL-2539) and K562 leukemia tumour cells (CCL-243) were obtained from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Co-Culture Assay, Control, Isolation, Cell Characterization

STAT1 and TUBB4A expression levels are significantly correlated and upregulated in melanoma. (A) Analysis of data in the Gene Expression Profiling Interactive Analysis 2 database revealed a significant elevation of STAT1 expression in melanoma tissues. Quantification of (B) STAT1 and (C) TUBB4A mRNA levels in 31 paired melanoma and normal tissue samples from patients with SKCM demonstrated a significant upregulation of both STAT1 and TUBB4A expression in melanoma tissues. (D) Correlation analysis of STAT1 and TUBB4A mRNA levels in melanoma samples showed a significant positive correlation. Comparative analysis of (E) STAT1 and (F) TUBB4A mRNA expression in normal HEM and melanoma cell lines revealed significantly higher expression in the melanoma cell lines. *P<0.05 between groups; **P<0.01 compared with HEM cells. HEM, human epidermal melanocytes; STAT1, signal transducer and activator of transcription 1; TUBB4A, tubulin β4A; TPM, transcripts per million; SKCM, skin cutaneous melanoma.

Journal: Molecular Medicine Reports

Article Title: STAT1 accelerates cutaneous melanoma progression through TUBB4A expression regulation

doi: 10.3892/mmr.2026.13828

Figure Lengend Snippet: STAT1 and TUBB4A expression levels are significantly correlated and upregulated in melanoma. (A) Analysis of data in the Gene Expression Profiling Interactive Analysis 2 database revealed a significant elevation of STAT1 expression in melanoma tissues. Quantification of (B) STAT1 and (C) TUBB4A mRNA levels in 31 paired melanoma and normal tissue samples from patients with SKCM demonstrated a significant upregulation of both STAT1 and TUBB4A expression in melanoma tissues. (D) Correlation analysis of STAT1 and TUBB4A mRNA levels in melanoma samples showed a significant positive correlation. Comparative analysis of (E) STAT1 and (F) TUBB4A mRNA expression in normal HEM and melanoma cell lines revealed significantly higher expression in the melanoma cell lines. *P<0.05 between groups; **P<0.01 compared with HEM cells. HEM, human epidermal melanocytes; STAT1, signal transducer and activator of transcription 1; TUBB4A, tubulin β4A; TPM, transcripts per million; SKCM, skin cutaneous melanoma.

Article Snippet: The melanoma cell lines A2058 (cat. no. CRL-3601), SK-MEL-1 (cat. no. HTB-67), A375 (cat. no. CRL-1619) and RPMI-7951 (cat. no. HTB-66), as well as normal human epidermal melanocytes (HEM; cat. no. PCS-200-013) and 293T cells (cat. no. CRL-3216) were obtained from American Type Culture Collection.

Techniques: Expressing, Gene Expression