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Procell Inc human blca cells t24

(A) IHC representation chart and western blot (WB) showed AKR1B1 expression in normal bladder tissue and <t>BLCA</t> tissue. Scale bar: 100μm. (B) WB detection of AKR1B1 relative expression in control, NC, and siAKR1B1 groups. (C) Colony formation experiment results with AKR1B1 expression. (D) Results of silencing AKR1B1 expression at different time points of CCK-8:24, 48, 72, 96h. (E) Edu assay showing proliferating <t>cells</t> <t>(T24</t> and 5637); Edu (red) and DAPI (blue) staining. Scale bar: 50μm. (F) Transwell assay results in control, NC, and siAKR1B1 groups. Scale bar: 100μm. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns p > 0.05.

Human Blca Cells T24, supplied by Procell Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 90 stars, based on 1 article reviews

human blca cells t24 - by Bioz Stars, 2026-03

90/100 stars

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1) Product Images from "Exploration and validation of a novel reactive oxygen species–related signature for predicting the prognosis and chemotherapy response of patients with bladder cancer"

Article Title: Exploration and validation of a novel reactive oxygen species–related signature for predicting the prognosis and chemotherapy response of patients with bladder cancer

Journal: Frontiers in Immunology

doi: 10.3389/fimmu.2024.1493528

(A) IHC representation chart and western blot (WB) showed AKR1B1 expression in normal bladder tissue and BLCA tissue. Scale bar: 100μm. (B) WB detection of AKR1B1 relative expression in control, NC, and siAKR1B1 groups. (C) Colony formation experiment results with AKR1B1 expression. (D) Results of silencing AKR1B1 expression at different time points of CCK-8:24, 48, 72, 96h. (E) Edu assay showing proliferating cells (T24 and 5637); Edu (red) and DAPI (blue) staining. Scale bar: 50μm. (F) Transwell assay results in control, NC, and siAKR1B1 groups. Scale bar: 100μm. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns p > 0.05.

Figure Legend Snippet: (A) IHC representation chart and western blot (WB) showed AKR1B1 expression in normal bladder tissue and BLCA tissue. Scale bar: 100μm. (B) WB detection of AKR1B1 relative expression in control, NC, and siAKR1B1 groups. (C) Colony formation experiment results with AKR1B1 expression. (D) Results of silencing AKR1B1 expression at different time points of CCK-8:24, 48, 72, 96h. (E) Edu assay showing proliferating cells (T24 and 5637); Edu (red) and DAPI (blue) staining. Scale bar: 50μm. (F) Transwell assay results in control, NC, and siAKR1B1 groups. Scale bar: 100μm. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns p > 0.05.

Techniques Used: Western Blot, Expressing, Control, CCK-8 Assay, EdU Assay, Staining, Transwell Assay

Image Search Results

BLCA cells exhibit remarkable tolerance to hypoxia and low glucose, adopting a quasi-quiescent and more aggressive invasive behavior (A) Hypoxia or low glucose (normoxia-Glc) significantly upregulates HIF-1α expression in BLCA cell lines, which is further enhanced when combined (hypoxia-Glc). (B) BLCA cells cultured in hypoxia and low glucose produce residual levels of lactate. Individually, these stressors induce the production of lactate. (C) Hypoxia and low glucose significantly suppress cell proliferation. Individually, low oxygen or low glucose inhibits cell proliferation. The combination of these stressors further exacerbates this effect in all cell lines. (D) BLCA cells maintain their viability under hypoxia and low glucose. The combined environmental stress from hypoxia and low glucose does not significantly impact the viability of 5637 and T24 cells. RT4 and HT1197 cells exhibit a 30%–45% reduction in viability under these conditions, suggesting a limited adaptive capacity. (E) BLCA cells display increased invasiveness under hypoxia or low glucose. This is significantly potentiated when both stimuli are combined. (F) BLCA cells demonstrate remarkable adaptability to microenvironmental changes with minimal impact on cell viability. Restoring oxygen and glucose levels does not affect cell viability, underscoring the high plasticity of these cells to endure drastic microenvironmental changes. (G) BLCA cells restore basal proliferation after 48 h of reoxygenation with glucose restoration. Both 5637 and T24 cells regain proliferative capacity, fully reinstating proliferation after 48 h, highlighting their plasticity in responding to microenvironmental challenges. (H) After 24 h of reoxygenation with glucose restoration, BLCA cells exhibit a significant reduction in invasion, which is fully restored under normoxia after 48 h. (I) Hypoxia and low glucose increase T24 cells' resistance to cisplatin across a wide range of concentrations, including its IC50, whereas 5637 cells remain unchanged. Error bars represent mean ± SD for three independent experiments. One-way ANOVA followed by Tukey’s multiple comparison test and the Mann-Whitney test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: BLCA cells exhibit remarkable tolerance to hypoxia and low glucose, adopting a quasi-quiescent and more aggressive invasive behavior (A) Hypoxia or low glucose (normoxia-Glc) significantly upregulates HIF-1α expression in BLCA cell lines, which is further enhanced when combined (hypoxia-Glc). (B) BLCA cells cultured in hypoxia and low glucose produce residual levels of lactate. Individually, these stressors induce the production of lactate. (C) Hypoxia and low glucose significantly suppress cell proliferation. Individually, low oxygen or low glucose inhibits cell proliferation. The combination of these stressors further exacerbates this effect in all cell lines. (D) BLCA cells maintain their viability under hypoxia and low glucose. The combined environmental stress from hypoxia and low glucose does not significantly impact the viability of 5637 and T24 cells. RT4 and HT1197 cells exhibit a 30%–45% reduction in viability under these conditions, suggesting a limited adaptive capacity. (E) BLCA cells display increased invasiveness under hypoxia or low glucose. This is significantly potentiated when both stimuli are combined. (F) BLCA cells demonstrate remarkable adaptability to microenvironmental changes with minimal impact on cell viability. Restoring oxygen and glucose levels does not affect cell viability, underscoring the high plasticity of these cells to endure drastic microenvironmental changes. (G) BLCA cells restore basal proliferation after 48 h of reoxygenation with glucose restoration. Both 5637 and T24 cells regain proliferative capacity, fully reinstating proliferation after 48 h, highlighting their plasticity in responding to microenvironmental challenges. (H) After 24 h of reoxygenation with glucose restoration, BLCA cells exhibit a significant reduction in invasion, which is fully restored under normoxia after 48 h. (I) Hypoxia and low glucose increase T24 cells' resistance to cisplatin across a wide range of concentrations, including its IC50, whereas 5637 cells remain unchanged. Error bars represent mean ± SD for three independent experiments. One-way ANOVA followed by Tukey’s multiple comparison test and the Mann-Whitney test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Expressing, Cell Culture, Comparison, MANN-WHITNEY

BLCA cell lines under hypoxia and low glucose experience profound transcriptome remodeling, linked to the acquisition of more aggressive phenotypes, which is supported by the poor prognosis observed in TCGA-BLCA patients (A) BLCA cell lines under hypoxia and low glucose display distinct transcriptomes but share common responses to these conditions. PCA for transcriptomics data reveals that PC1 (94% variance) primarily distinguishes differences between cell lines, whereas PC2 (5% variance) highlights marked changes between normoxic and stressed cells. (B) The volcano plot showcases global transcriptional changes between normoxia and hypoxia plus low glucose. Exposure to these stressors alters the expression of 4,044 genes (1,722 upregulated, 2,322 downregulated), indicating significant transcriptome remodeling. (C) Bi-clustering heatmap of the top 30 differentially expressed genes illustrates co-regulation under stress, supporting proliferation arrest, resistance to cell death, and invasion. Heatmap plots log2 transformed expression values of genes in samples. (D) Enrichment analysis of GO terms for differentially expressed genes reveals alterations in key pathways associated with cell-cell adhesion, cell proliferation, and resistance to cell death. (E) Prognostic evaluation identifies a hypoxia and glucose-deprivation-linked four-gene signature ( TAGLN high ; SLC2A3 high ; TRIB3 high ; TMEM158 high ). Univariate Cox regression analysis of the top 30 differentially expressed genes identifies seven genes associated with OS. Higher expression levels of four genes, upregulated under hypoxia and low glucose, significantly correlate with poor OS, constituting a stress signature. (F) Validation of the prognosis significance of the hypoxia-related four-gene signature in BLCA patients from TCGA. Kaplan-Meier curves of OS and PFS show significantly worse clinical outcomes for patients displaying the stress-related gene signature compared to the remaining patients in the cohort. (G) Bi-clustering heatmap showing the association between the stress-related signature and bladder tumors. Heatmap plots log2 transformed expression values of the four hypoxia-related differentially expressed genes, showing clear differentiation between cancer and healthy bladder samples.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: BLCA cell lines under hypoxia and low glucose experience profound transcriptome remodeling, linked to the acquisition of more aggressive phenotypes, which is supported by the poor prognosis observed in TCGA-BLCA patients (A) BLCA cell lines under hypoxia and low glucose display distinct transcriptomes but share common responses to these conditions. PCA for transcriptomics data reveals that PC1 (94% variance) primarily distinguishes differences between cell lines, whereas PC2 (5% variance) highlights marked changes between normoxic and stressed cells. (B) The volcano plot showcases global transcriptional changes between normoxia and hypoxia plus low glucose. Exposure to these stressors alters the expression of 4,044 genes (1,722 upregulated, 2,322 downregulated), indicating significant transcriptome remodeling. (C) Bi-clustering heatmap of the top 30 differentially expressed genes illustrates co-regulation under stress, supporting proliferation arrest, resistance to cell death, and invasion. Heatmap plots log2 transformed expression values of genes in samples. (D) Enrichment analysis of GO terms for differentially expressed genes reveals alterations in key pathways associated with cell-cell adhesion, cell proliferation, and resistance to cell death. (E) Prognostic evaluation identifies a hypoxia and glucose-deprivation-linked four-gene signature ( TAGLN high ; SLC2A3 high ; TRIB3 high ; TMEM158 high ). Univariate Cox regression analysis of the top 30 differentially expressed genes identifies seven genes associated with OS. Higher expression levels of four genes, upregulated under hypoxia and low glucose, significantly correlate with poor OS, constituting a stress signature. (F) Validation of the prognosis significance of the hypoxia-related four-gene signature in BLCA patients from TCGA. Kaplan-Meier curves of OS and PFS show significantly worse clinical outcomes for patients displaying the stress-related gene signature compared to the remaining patients in the cohort. (G) Bi-clustering heatmap showing the association between the stress-related signature and bladder tumors. Heatmap plots log2 transformed expression values of the four hypoxia-related differentially expressed genes, showing clear differentiation between cancer and healthy bladder samples.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Expressing, Transformation Assay, Biomarker Discovery

Hypoxia and low glucose shift BLCA cell metabolism from glycolytic to lipolytic, increasing lipid droplet formation and reducing the number of active mitochondria (A–C) PLS-DA analysis reveals similar metabolic responses in 5637 and T24 cells under microenvironmental stress (A). Volcano plot highlights significant metabolome alterations in response to hypoxia and low glucose (B). Downregulated metabolites include UDP-Glc, UDP-GalNAc, gluconic acid, and citric acid, whereas increased metabolites indicate active fatty acid transport and β-oxidation (C). Significant reduction in key metabolites linked to nucleotide, amino acids, Krebs cycle, and lipid metabolism was observed, consistent with catabolic metabolism. An exception is the accumulation of long fatty acid acylcarnitine for transfer across the inner mitochondrial membrane for β-oxidation. (D) Pathway enrichment analysis supports fatty acid β-oxidation as the primary bioenergetic pathway in stressed cells. Key metabolic pathways, including carnitine biosynthesis and lysine/methionine degradation, contribute to fatty acid β-oxidation. (E) Hypoxia and low glucose induce lysine and methionine degradation to support acylcarnitine biosynthesis and lipid β-oxidation. (F) Joint pathway analysis incorporating transcriptomics and metabolomics studies supports changes from glycolytic to lipolytic metabolism, impacting nucleotides and sugars biosynthesis, including O -GalNAc glycans and protein O -glycosylation. (G and H) Hypoxia and low glucose increase AMP/ATP ratio (G) and activate AMPK by phosphorylation (H), indicating impaired oxidative phosphorylation and potential catabolic processes, including mitophagy. (I) Citrate synthase activity decreases under hypoxia and low glucose, suggesting a reduction in functional mitochondria. (J) TEM analysis reveals major morphological changes, including compromised mitochondria, lipid droplets, peridroplet mitochondria, membrane vesicles, and increased shedding of vesicles, indicating membrane activity changes under stress. Error bars represent mean ± SD for three independent experiments. Mann-Whitney test was used for statistical analysis. Results were considered statistically significant when p < 0.05.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: Hypoxia and low glucose shift BLCA cell metabolism from glycolytic to lipolytic, increasing lipid droplet formation and reducing the number of active mitochondria (A–C) PLS-DA analysis reveals similar metabolic responses in 5637 and T24 cells under microenvironmental stress (A). Volcano plot highlights significant metabolome alterations in response to hypoxia and low glucose (B). Downregulated metabolites include UDP-Glc, UDP-GalNAc, gluconic acid, and citric acid, whereas increased metabolites indicate active fatty acid transport and β-oxidation (C). Significant reduction in key metabolites linked to nucleotide, amino acids, Krebs cycle, and lipid metabolism was observed, consistent with catabolic metabolism. An exception is the accumulation of long fatty acid acylcarnitine for transfer across the inner mitochondrial membrane for β-oxidation. (D) Pathway enrichment analysis supports fatty acid β-oxidation as the primary bioenergetic pathway in stressed cells. Key metabolic pathways, including carnitine biosynthesis and lysine/methionine degradation, contribute to fatty acid β-oxidation. (E) Hypoxia and low glucose induce lysine and methionine degradation to support acylcarnitine biosynthesis and lipid β-oxidation. (F) Joint pathway analysis incorporating transcriptomics and metabolomics studies supports changes from glycolytic to lipolytic metabolism, impacting nucleotides and sugars biosynthesis, including O -GalNAc glycans and protein O -glycosylation. (G and H) Hypoxia and low glucose increase AMP/ATP ratio (G) and activate AMPK by phosphorylation (H), indicating impaired oxidative phosphorylation and potential catabolic processes, including mitophagy. (I) Citrate synthase activity decreases under hypoxia and low glucose, suggesting a reduction in functional mitochondria. (J) TEM analysis reveals major morphological changes, including compromised mitochondria, lipid droplets, peridroplet mitochondria, membrane vesicles, and increased shedding of vesicles, indicating membrane activity changes under stress. Error bars represent mean ± SD for three independent experiments. Mann-Whitney test was used for statistical analysis. Results were considered statistically significant when p < 0.05.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Membrane, Glycoproteomics, Phospho-proteomics, Activity Assay, Functional Assay, MANN-WHITNEY

Hypoxia and low glucose impair O -glycans extension in BLCA, originating a simple cancer cell glycophenotype (A) BLCA cells exposed to hypoxia and low glucose exhibit less abundant, simpler, and shorter glycomes, lacking extensions beyond core 1 structures. nanoLC-MS/MS analysis shows that this glycophenotype is characterized by sialylated T antigens and core 3, likely due to decreased typical core 1 and 2 structures. DFX-treated cells, stabilizing HIF-1α, show no significant alterations in the glycome, suggesting that changes observed in stressed cells are not driven by HIF-1α. (B) Lectin affinity studies show significant upregulation of Tn and sialylated T antigens (recognized by PNA lectin after Neuraminidase [NeuAse] digestion) under stress, in accordance with MS-based glycomics. Notably, core 3 O -glycans (evaluated by GSL II lectin after PNGase F digestion) remain unchanged, highlighting that cellular stress primarily suppresses core 1/2 O -glycans, rather than increasing core 3 O -glycans. (C) Glucose suppression is the primary driver of glycome remodeling, which can be reversed by reoxygenation and restoration of glucose. (D) Glycogene remodeling is primarily driven by the combined effects of hypoxia and glucose deprivation and leads to a premature halt in glycans extension beyond core 1. C1GALT1C1 , necessary for core 1 biosynthesis, is downregulated, whereas ST3GAL1 , 3 , and 4 are overexpressed, increasing sialylated T antigens and inhibiting core 2 formation. Downregulation of GCNT4 also contributes to core 2 inhibition. Interestingly, elevated GCNT1 and GCNT3 potentially counterbalance core 2 suppression. (E) Quantification of key enzymes involved in O -glycan elongation (C1GalT1; Cosmc; BGnT-6; C2GNT; ST3Gal-I) shows significant upregulation of ST3Gal-1 in stressed cells, consistent with transcriptomics. The others remain unchanged, indicating distinct regulation between glycogenes and glycosyltransferases under these conditions. Bold circles and triangles represent statistically significant changes in T24 and 5637 cell lines, respectively. Error bars represent mean ± SD for three independent experiments. Mann-Whitney Test was used for statistical analysis. Results were considered statistically significant when p < 0.05.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: Hypoxia and low glucose impair O -glycans extension in BLCA, originating a simple cancer cell glycophenotype (A) BLCA cells exposed to hypoxia and low glucose exhibit less abundant, simpler, and shorter glycomes, lacking extensions beyond core 1 structures. nanoLC-MS/MS analysis shows that this glycophenotype is characterized by sialylated T antigens and core 3, likely due to decreased typical core 1 and 2 structures. DFX-treated cells, stabilizing HIF-1α, show no significant alterations in the glycome, suggesting that changes observed in stressed cells are not driven by HIF-1α. (B) Lectin affinity studies show significant upregulation of Tn and sialylated T antigens (recognized by PNA lectin after Neuraminidase [NeuAse] digestion) under stress, in accordance with MS-based glycomics. Notably, core 3 O -glycans (evaluated by GSL II lectin after PNGase F digestion) remain unchanged, highlighting that cellular stress primarily suppresses core 1/2 O -glycans, rather than increasing core 3 O -glycans. (C) Glucose suppression is the primary driver of glycome remodeling, which can be reversed by reoxygenation and restoration of glucose. (D) Glycogene remodeling is primarily driven by the combined effects of hypoxia and glucose deprivation and leads to a premature halt in glycans extension beyond core 1. C1GALT1C1 , necessary for core 1 biosynthesis, is downregulated, whereas ST3GAL1 , 3 , and 4 are overexpressed, increasing sialylated T antigens and inhibiting core 2 formation. Downregulation of GCNT4 also contributes to core 2 inhibition. Interestingly, elevated GCNT1 and GCNT3 potentially counterbalance core 2 suppression. (E) Quantification of key enzymes involved in O -glycan elongation (C1GalT1; Cosmc; BGnT-6; C2GNT; ST3Gal-I) shows significant upregulation of ST3Gal-1 in stressed cells, consistent with transcriptomics. The others remain unchanged, indicating distinct regulation between glycogenes and glycosyltransferases under these conditions. Bold circles and triangles represent statistically significant changes in T24 and 5637 cell lines, respectively. Error bars represent mean ± SD for three independent experiments. Mann-Whitney Test was used for statistical analysis. Results were considered statistically significant when p < 0.05.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Tandem Mass Spectroscopy, Inhibition, Glycoproteomics, MANN-WHITNEY

Hypoxic BLCA, characterized by high nuclear HIF-1α expression and low proliferation, shares malignant molecular features with hypoxic and glucose-deprived cells in vitro , including simple glycophenotypes (A and B) Roughly 10% of MIBC tumors display a hypoxic fingerprint (HIF-1α positive /Ki-67 low ) that was not observed in NMIBC and most MIBC tumors (HIF-1α negative /Ki-67 high ), indicating a potential link to aggressiveness. (C) Hypoxic tumors display significantly higher AMPK phosphorylation compared to proliferative cases, denoting a catabolic state. (D) Hypoxic tumors show distinct cellular signaling pathway activation compared to proliferative tumors. PCA for phosphoproteomics data indicates that PC1 (58% variance) primarily separates hypoxic from proliferative tumors, whereas PC2 (15% variance) highlights marked differences among hypoxic tumors. (E) Kinase-Substrate enrichment analysis supports major cell rewiring in hypoxic tumors. Kinases color-coded in red are significantly activated, whereas blue is significantly inactivated. (F) Hypoxic tumors share common kinase activation patterns with stressed BLCA cells in vitro . (G) KEGG pathway enrichment analysis indicates significant alterations in cell signaling pathways, promoting cell motility, cellular senescence, and autophagy in hypoxic tumors as found in stressed cells in vitro . (H) Hypoxic tumors present simple O -glycophenotypes compared to proliferative tumors. nanoLC-MS/MS reveals more homogeneous O -glycome in hypoxic tumors with scarce core 2 glycans. We represent the most abundant structures also found in cell lines, keeping reference to their original relative abundance in relation to all identified glycan species. (I) Hypoxic tumors N -glycome is enriched for oligomannose N -glycans, whereas proliferative tumors are enriched for complex N -glycans. (J and K) Hypoxic tumors show higher levels of Tn and sialylated T antigens and lower levels of sialylated Lewis antigens in O -glycans compared to proliferative tumors, reinforcing the primary suppression of O -glycan extension. NeuAse means sialidase neuraminidase. (L) In hypoxic tumors, Tn and sialylated T antigens co-localize with high HIF-1α. Normoxic, proliferative tumors lack HIF-1α and show low levels of sialylated T antigens and no Tn antigens. Healthy urothelium from non-cancerous individuals served as a negative control for HIF-1α, low Tn, and sialylated T antigens expression. Unpaired t test and Mann-Whitney test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: Hypoxic BLCA, characterized by high nuclear HIF-1α expression and low proliferation, shares malignant molecular features with hypoxic and glucose-deprived cells in vitro , including simple glycophenotypes (A and B) Roughly 10% of MIBC tumors display a hypoxic fingerprint (HIF-1α positive /Ki-67 low ) that was not observed in NMIBC and most MIBC tumors (HIF-1α negative /Ki-67 high ), indicating a potential link to aggressiveness. (C) Hypoxic tumors display significantly higher AMPK phosphorylation compared to proliferative cases, denoting a catabolic state. (D) Hypoxic tumors show distinct cellular signaling pathway activation compared to proliferative tumors. PCA for phosphoproteomics data indicates that PC1 (58% variance) primarily separates hypoxic from proliferative tumors, whereas PC2 (15% variance) highlights marked differences among hypoxic tumors. (E) Kinase-Substrate enrichment analysis supports major cell rewiring in hypoxic tumors. Kinases color-coded in red are significantly activated, whereas blue is significantly inactivated. (F) Hypoxic tumors share common kinase activation patterns with stressed BLCA cells in vitro . (G) KEGG pathway enrichment analysis indicates significant alterations in cell signaling pathways, promoting cell motility, cellular senescence, and autophagy in hypoxic tumors as found in stressed cells in vitro . (H) Hypoxic tumors present simple O -glycophenotypes compared to proliferative tumors. nanoLC-MS/MS reveals more homogeneous O -glycome in hypoxic tumors with scarce core 2 glycans. We represent the most abundant structures also found in cell lines, keeping reference to their original relative abundance in relation to all identified glycan species. (I) Hypoxic tumors N -glycome is enriched for oligomannose N -glycans, whereas proliferative tumors are enriched for complex N -glycans. (J and K) Hypoxic tumors show higher levels of Tn and sialylated T antigens and lower levels of sialylated Lewis antigens in O -glycans compared to proliferative tumors, reinforcing the primary suppression of O -glycan extension. NeuAse means sialidase neuraminidase. (L) In hypoxic tumors, Tn and sialylated T antigens co-localize with high HIF-1α. Normoxic, proliferative tumors lack HIF-1α and show low levels of sialylated T antigens and no Tn antigens. Healthy urothelium from non-cancerous individuals served as a negative control for HIF-1α, low Tn, and sialylated T antigens expression. Unpaired t test and Mann-Whitney test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Expressing, In Vitro, Phospho-proteomics, Activation Assay, Protein-Protein interactions, Tandem Mass Spectroscopy, Glycoproteomics, Negative Control, MANN-WHITNEY

Hypoxia and low-glucose-induced simple glycophenotypes drive relevant cancer-associated hallmarks (A and B) T24 C1GALT1 KOs show complete abrogation of O -glycans extension beyond the Tn antigen, mirroring a major alteration observed in hypoxic tumors. Glycoengineered cells homogeneously express the Tn antigen and show low levels of core 3. Mock controls' glycosylation closely resembles T24 wild-type cells. (C) C1GALT1 KOs display reduced proliferation compared to controls under normoxia. Collectively, altered glycosylation impacts proliferation more when compared to hypoxia and glucose deprivation. (D) Under normoxia and hypoxia with glucose deprivation, C1GALT1 KOs glycoengineered cells display significantly enhanced invasion, suggesting a critical role of C1GALT1 in modulating invasive behavior under stress. (E and F) C1GALT1 KOs demonstrate higher resistance to cisplatin (E) and anoikis compared to mock controls (F). (G and H) In CAMs, C1GALT1 KOs give rise to smaller tumors (G), in agreement with proliferation studies in vitro (C), showing less cohesive features and invasive patterns compared to control (H). (I and J) T24 GCNT1 KOs exhibit complete abrogation of O -glycans extension beyond core 1, mirroring another major alteration observed in hypoxic tumors. As a result, glycoengineered cells express high levels of sialylated T antigens, namely sialyl-T, but do not present core 2-derived glycans. Mock controls' glycosylation closely resembles T24 wild-type cells. (K and L) GCNT1 KOs display reduced proliferation compared to controls (K) and increased invasion (L) under normoxia, resembling C1GALT1 KOs. A higher invasion is also observed under hypoxia-Glc. (M and N) GCNT1 KOs demonstrate similar resistance to cisplatin (M) but higher resistance to anoikis compared to mock controls (N). (O and P) In CAMs, GCNT1 KOs give rise to smaller (O) and more invasive tumors compared to controls (P). Error bars represent mean ± SD for three independent experiments. Unpaired t test, two-way ANOVA followed by Tukey’s multiple comparison test, and Wilcoxon test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet: Hypoxia and low-glucose-induced simple glycophenotypes drive relevant cancer-associated hallmarks (A and B) T24 C1GALT1 KOs show complete abrogation of O -glycans extension beyond the Tn antigen, mirroring a major alteration observed in hypoxic tumors. Glycoengineered cells homogeneously express the Tn antigen and show low levels of core 3. Mock controls' glycosylation closely resembles T24 wild-type cells. (C) C1GALT1 KOs display reduced proliferation compared to controls under normoxia. Collectively, altered glycosylation impacts proliferation more when compared to hypoxia and glucose deprivation. (D) Under normoxia and hypoxia with glucose deprivation, C1GALT1 KOs glycoengineered cells display significantly enhanced invasion, suggesting a critical role of C1GALT1 in modulating invasive behavior under stress. (E and F) C1GALT1 KOs demonstrate higher resistance to cisplatin (E) and anoikis compared to mock controls (F). (G and H) In CAMs, C1GALT1 KOs give rise to smaller tumors (G), in agreement with proliferation studies in vitro (C), showing less cohesive features and invasive patterns compared to control (H). (I and J) T24 GCNT1 KOs exhibit complete abrogation of O -glycans extension beyond core 1, mirroring another major alteration observed in hypoxic tumors. As a result, glycoengineered cells express high levels of sialylated T antigens, namely sialyl-T, but do not present core 2-derived glycans. Mock controls' glycosylation closely resembles T24 wild-type cells. (K and L) GCNT1 KOs display reduced proliferation compared to controls (K) and increased invasion (L) under normoxia, resembling C1GALT1 KOs. A higher invasion is also observed under hypoxia-Glc. (M and N) GCNT1 KOs demonstrate similar resistance to cisplatin (M) but higher resistance to anoikis compared to mock controls (N). (O and P) In CAMs, GCNT1 KOs give rise to smaller (O) and more invasive tumors compared to controls (P). Error bars represent mean ± SD for three independent experiments. Unpaired t test, two-way ANOVA followed by Tukey’s multiple comparison test, and Wilcoxon test were used for statistical analysis. Results were considered statistically significant when p < 0.05.

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Glycoproteomics, In Vitro, Control, Derivative Assay, Comparison

Journal: iScience

Article Title: Multilevel plasticity and altered glycosylation drive aggressiveness in hypoxic and glucose-deprived bladder cancer cells

doi: 10.1016/j.isci.2025.111758

Figure Lengend Snippet:

Article Snippet: Human BLCA cell line T24 (white female patient) , ATCC , HTB-4TM.

Techniques: Control, Purification, Recombinant, Plasmid Preparation, Electron Microscopy, Transfection, Staining, Enzyme-linked Immunosorbent Assay, Flow Cytometry, ATP Assay, Phospho-proteomics, Software, Sterility

Journal: Frontiers in Immunology

Article Title: Exploration and validation of a novel reactive oxygen species–related signature for predicting the prognosis and chemotherapy response of patients with bladder cancer

doi: 10.3389/fimmu.2024.1493528

Figure Lengend Snippet: (A) IHC representation chart and western blot (WB) showed AKR1B1 expression in normal bladder tissue and BLCA tissue. Scale bar: 100μm. (B) WB detection of AKR1B1 relative expression in control, NC, and siAKR1B1 groups. (C) Colony formation experiment results with AKR1B1 expression. (D) Results of silencing AKR1B1 expression at different time points of CCK-8:24, 48, 72, 96h. (E) Edu assay showing proliferating cells (T24 and 5637); Edu (red) and DAPI (blue) staining. Scale bar: 50μm. (F) Transwell assay results in control, NC, and siAKR1B1 groups. Scale bar: 100μm. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns p > 0.05.

Article Snippet: Human BLCA cells (T24 and 5637) were procured from Procell Life Science & Technology Company (Hubei, China).

Techniques: Western Blot, Expressing, Control, CCK-8 Assay, EdU Assay, Staining, Transwell Assay

Elevated OTUB1 is involved in the tumorigenesis of BLCA in vivo . Flow chart for the mouse model of spontaneous BLCA by feeding 0.1% BNN in water, these mice were treated with or without 0.1% BNN daily for 3 months. After stopping feeding BNN, all mice were divided into two groups according to time (1-6 months group and 7-12 months group). These bladders were removed and further handled for H&E staining and immunohistochemical staining (OTUB1 and ki-67). The left group from top to bottom: normal bladder structure, bladder carcinoma in situ , invasive BLCA; the Middle group from top to bottom: IHC staining for OTUB1 according to the sequence of H&E staining; Right group from top to bottom: IHC staining for ki-67 according to the sequence of H&E staining.

Journal: International Journal of Biological Sciences

Article Title: Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway

doi: 10.7150/ijbs.94013

Figure Lengend Snippet: Elevated OTUB1 is involved in the tumorigenesis of BLCA in vivo . Flow chart for the mouse model of spontaneous BLCA by feeding 0.1% BNN in water, these mice were treated with or without 0.1% BNN daily for 3 months. After stopping feeding BNN, all mice were divided into two groups according to time (1-6 months group and 7-12 months group). These bladders were removed and further handled for H&E staining and immunohistochemical staining (OTUB1 and ki-67). The left group from top to bottom: normal bladder structure, bladder carcinoma in situ , invasive BLCA; the Middle group from top to bottom: IHC staining for OTUB1 according to the sequence of H&E staining; Right group from top to bottom: IHC staining for ki-67 according to the sequence of H&E staining.

Article Snippet: Human BLCA cell line (T24, 5637, BIU-87, EJ, 253J-BV) and human bladder epithelial immortalized cell (SV-HUC) were purchased from ATCC cell bank (America).

Techniques: In Vivo, Staining, Immunohistochemical staining, In Situ, Immunohistochemistry, Sequencing

OTUB1 facilitates the proliferation and migration of BLCA. A. Relative OTUB1 expression in bladder epithelial immortalized cell SV-HUC and several BLCA cells by western blot and qRT-PCR. B, C. Relative OTUB1 expression following overexpressed or knockdown OTUB1 by western blot. D, F, G. MTT assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cells following overexpressed or knockdown OTUB1. E. Transwell assay showed the invasion ability of BLCA cells following overexpressed or knockdown OTUB1. H, I, J. Cell cycle assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cell after transfecting with shOTUB1 lentivirus. K. Relative cell cycle-related markers expression following overexpressed or knockdown OTUB1 by western blot.

Journal: International Journal of Biological Sciences

Article Title: Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway

doi: 10.7150/ijbs.94013

Figure Lengend Snippet: OTUB1 facilitates the proliferation and migration of BLCA. A. Relative OTUB1 expression in bladder epithelial immortalized cell SV-HUC and several BLCA cells by western blot and qRT-PCR. B, C. Relative OTUB1 expression following overexpressed or knockdown OTUB1 by western blot. D, F, G. MTT assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cells following overexpressed or knockdown OTUB1. E. Transwell assay showed the invasion ability of BLCA cells following overexpressed or knockdown OTUB1. H, I, J. Cell cycle assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cell after transfecting with shOTUB1 lentivirus. K. Relative cell cycle-related markers expression following overexpressed or knockdown OTUB1 by western blot.

Article Snippet: Human BLCA cell line (T24, 5637, BIU-87, EJ, 253J-BV) and human bladder epithelial immortalized cell (SV-HUC) were purchased from ATCC cell bank (America).

Techniques: Migration, Expressing, Western Blot, Quantitative RT-PCR, Knockdown, MTT Assay, Transwell Assay, Cell Cycle Assay

OTUB1 promotes the progression of BLCA depending on β-catenin/RIPK3/MLKL/necroptosis signaling pathway. A. Relative expression of OTUB1, β-catenin and downstream targets following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; relative expression of OTUB1, β-catenin and downstream targets following knockdown OTUB1 and/or overexpressed β-catenin. B. The RNA expression of OTUB1, β-catenin, RIPK3 and MLKL in elevated OTUB1, β-catenin groups with or without XAV-939 treatment. C, E, F. MTT assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cell following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; coupled with that following knockdown OTUB1 and/or overexpressed β-catenin. D. Transwell assay showed the invasion ability of BLCA cells following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; coupled with that following knockdown OTUB1 and/or overexpressed β-catenin.

Journal: International Journal of Biological Sciences

Article Title: Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway

doi: 10.7150/ijbs.94013

Figure Lengend Snippet: OTUB1 promotes the progression of BLCA depending on β-catenin/RIPK3/MLKL/necroptosis signaling pathway. A. Relative expression of OTUB1, β-catenin and downstream targets following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; relative expression of OTUB1, β-catenin and downstream targets following knockdown OTUB1 and/or overexpressed β-catenin. B. The RNA expression of OTUB1, β-catenin, RIPK3 and MLKL in elevated OTUB1, β-catenin groups with or without XAV-939 treatment. C, E, F. MTT assay, clone formation experiments and healing assay showed the proliferation ability of BLCA cell following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; coupled with that following knockdown OTUB1 and/or overexpressed β-catenin. D. Transwell assay showed the invasion ability of BLCA cells following overexpressed OTUB1 with or without XAV-939 (5uM, 10uM) treatment; coupled with that following knockdown OTUB1 and/or overexpressed β-catenin.

Article Snippet: Human BLCA cell line (T24, 5637, BIU-87, EJ, 253J-BV) and human bladder epithelial immortalized cell (SV-HUC) were purchased from ATCC cell bank (America).

Techniques: Expressing, Knockdown, RNA Expression, MTT Assay, Transwell Assay

OTUB1 is involved in cisplatin resistance of BLCA through β-catenin stabilization. A. Cell survival assay was determined in T24 control cell and T24 cisplatin-resistance cell. B. The changes in cell morphology between the T24 control cell and the T24 cisplatin-resistance cell. C. Relative expression of several chemoresistance markers (including MDR1, BCRP and YB-1) in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. D. Relative expression of OTUB1 in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. E. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream proteins (including AXIN-2, C-myc, cyclin D1 and TCF1) in T24 cisplatin-resistance cells treated with gradient cisplatin concentration. F. Immunoprecipitation assay showed the relationship between OTUB1 and β-catenin in T24 cisplatin-resistance cells. G. Immunoprecipitation assay showed that gradient cisplatin concentration promotes the interaction between OTUB1 and β-catenin, and restrains the ubiquitination of β-catenin. H. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream targets following elevated OTUB1, β-catenin with or without XAV-939 treatment in T24 cisplatin-resistance cell (control, OTUB1, OTUB1/XAV-939, β-catenin). I. Cell survival assay was determined in T24 cisplatin-resistance cells following overexpressed OTUB1 with or without 10uM XAV-939 (or knockdown OTUB1 with or without overexpressed β-catenin). J. Knockdown OTUB1 restrains the growth in T24 cisplatin-resistance mice bladder tumor in vivo .

Journal: International Journal of Biological Sciences

Article Title: Target deubiquitinase OTUB1 as a therapeatic strategy for BLCA via β-catenin/necroptosis signal pathway

doi: 10.7150/ijbs.94013

Figure Lengend Snippet: OTUB1 is involved in cisplatin resistance of BLCA through β-catenin stabilization. A. Cell survival assay was determined in T24 control cell and T24 cisplatin-resistance cell. B. The changes in cell morphology between the T24 control cell and the T24 cisplatin-resistance cell. C. Relative expression of several chemoresistance markers (including MDR1, BCRP and YB-1) in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. D. Relative expression of OTUB1 in T24 control cell and T24 cisplatin-resistance cell with or without cisplatin treatment. E. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream proteins (including AXIN-2, C-myc, cyclin D1 and TCF1) in T24 cisplatin-resistance cells treated with gradient cisplatin concentration. F. Immunoprecipitation assay showed the relationship between OTUB1 and β-catenin in T24 cisplatin-resistance cells. G. Immunoprecipitation assay showed that gradient cisplatin concentration promotes the interaction between OTUB1 and β-catenin, and restrains the ubiquitination of β-catenin. H. Relative expression of OTUB1, necroptosis-related markers (such as RIPK3, MLKL and P-MLKL), β-catenin and downstream targets following elevated OTUB1, β-catenin with or without XAV-939 treatment in T24 cisplatin-resistance cell (control, OTUB1, OTUB1/XAV-939, β-catenin). I. Cell survival assay was determined in T24 cisplatin-resistance cells following overexpressed OTUB1 with or without 10uM XAV-939 (or knockdown OTUB1 with or without overexpressed β-catenin). J. Knockdown OTUB1 restrains the growth in T24 cisplatin-resistance mice bladder tumor in vivo .

Article Snippet: Human BLCA cell line (T24, 5637, BIU-87, EJ, 253J-BV) and human bladder epithelial immortalized cell (SV-HUC) were purchased from ATCC cell bank (America).

Techniques: Clonogenic Cell Survival Assay, Control, Expressing, Concentration Assay, Immunoprecipitation, Ubiquitin Proteomics, Knockdown, In Vivo

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