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t24 (ATCC)

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ATCC t24
T24, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 2689 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/t24/product/ATCC
Average 98 stars, based on 2689 article reviews

t24 - by Bioz Stars, 2026-06

98/100 stars

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Effect of ARAF on the proliferation of T24 cells. (A) RT-qPCR analysis of si-ARAF transfection efficiency. (B and C) Western blot analysis of si-ARAF transfection efficiency. (D) EdU fluorescence assay showing proliferating cells. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ***p<0.001, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Effect of ARAF on the proliferation of T24 cells. (A) RT-qPCR analysis of si-ARAF transfection efficiency. (B and C) Western blot analysis of si-ARAF transfection efficiency. (D) EdU fluorescence assay showing proliferating cells. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ***p<0.001, ****p<0.0001.

Article Snippet: The human ureter epithelial immortalized cell line SV-HUC-1 (CL-0222) and human bladder cancer cell lines T24 (CL-0227) and J82 (CL-0125) were purchased from Wuhan Procell Biological Company.

Techniques: Quantitative RT-PCR, Transfection, Western Blot, Fluorescence

Effect of ARAF on apoptosis of T24 cells. (A and B) Flow cytometry analysis of apoptosis levels. (C and D) Protein expression of cleaved-caspase 3 and total caspase 3. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. **p<0.01, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Effect of ARAF on apoptosis of T24 cells. (A and B) Flow cytometry analysis of apoptosis levels. (C and D) Protein expression of cleaved-caspase 3 and total caspase 3. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. **p<0.01, ****p<0.0001.

Techniques: Flow Cytometry, Expressing

Effect of ARAF on the metastatic capacity of T24 cells. (A and B) Quantification of migrating cells. (A and C) Quantification of invading cells. (D and E) Expression of EMT-related proteins in T24 cells. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Effect of ARAF on the metastatic capacity of T24 cells. (A and B) Quantification of migrating cells. (A and C) Quantification of invading cells. (D and E) Expression of EMT-related proteins in T24 cells. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ****p<0.0001.

Techniques: Expressing

Effect of ARAF on the p38 MAPK pathway in T24 cells. (A) The level of p-p38, p38, p-ERK, ERK, p-MEK, MEK in T24 cells was determined by western blot assay. (B) p-p38/p38 ratio. (C) p-ERK/ERK ratio. (D) p-MEK/MEK ratio. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ***p<0.001, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Effect of ARAF on the p38 MAPK pathway in T24 cells. (A) The level of p-p38, p38, p-ERK, ERK, p-MEK, MEK in T24 cells was determined by western blot assay. (B) p-p38/p38 ratio. (C) p-ERK/ERK ratio. (D) p-MEK/MEK ratio. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using one-way ANOVA. ***p<0.001, ****p<0.0001.

Techniques: Western Blot

Anisomycin activated p38 MAPK pathway in si-ARAF transfected T24 cells. (A) The level of p-p38, p38, p-ERK, ERK, p-MEK, MEK in T24 cells was determined by western blot assay. (B) p-p38/p38 ratio. (C) p-ERK/ERK ratio. (D) p-MEK/MEK ratio. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. ***p<0.001, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Anisomycin activated p38 MAPK pathway in si-ARAF transfected T24 cells. (A) The level of p-p38, p38, p-ERK, ERK, p-MEK, MEK in T24 cells was determined by western blot assay. (B) p-p38/p38 ratio. (C) p-ERK/ERK ratio. (D) p-MEK/MEK ratio. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. ***p<0.001, ****p<0.0001.

Techniques: Transfection, Western Blot

Anisomycin reversed the effect of ARAF on T24 cell proliferation and apoptosis. (A) EdU fluorescence for cell proliferation capacity. (B) The apoptotic rate of T24 cells. (C and D) The protein level of Cleaved-caspase3 and Caspase3. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. **p<0.01, ***p<0.001, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Anisomycin reversed the effect of ARAF on T24 cell proliferation and apoptosis. (A) EdU fluorescence for cell proliferation capacity. (B) The apoptotic rate of T24 cells. (C and D) The protein level of Cleaved-caspase3 and Caspase3. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. **p<0.01, ***p<0.001, ****p<0.0001.

Techniques: Fluorescence

Anisomycin reversed the effect of ARAF on T24 cell metastasis and EMT. (A–C) The migratory and invasive ability of T24 cells. (D–F) The protein level of E-cadherin and N-cadherin. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. **p<0.01, ****p<0.0001.

Journal: Open Medicine

Article Title: ARAF regulates malignant progression of bladder cancer through the p38MAPK pathway

doi: 10.1515/med-2026-1422

Figure Lengend Snippet: Anisomycin reversed the effect of ARAF on T24 cell metastasis and EMT. (A–C) The migratory and invasive ability of T24 cells. (D–F) The protein level of E-cadherin and N-cadherin. Data are presented as mean ± SD from three independent biological replicates. Statistical analysis was performed using Student’s t-test. **p<0.01, ****p<0.0001.

Techniques:

Betulinic acid (BA) enhances tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated cytotoxicity in T24 human bladder cancer cells. T24 cells were treated with the indicated concentrations of BA and TRAIL alone or in combination for 24 h. (A, B) After treatment, cell viability was assessed via 3′-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. (C) Morphological changes in the cells treated with BA and TRAIL alone or in combination were observed under an inverted microscope. (D, E) After 4′,6-diamidino-2-phenylindole (DAPI) staining, nuclear morphological changes were observed under a fluorescence microscope (D), and the frequency of cells with chromatin condensation and fragmentation was determined (E). (F, G) Flow cytometry was performed after propidium iodide (PI) staining. Representative histograms (F) and the frequency of cells in the sub-G1 phase (G) are shown. * p <0.05, ** p <0.01, and *** p <0.001 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3).

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Betulinic acid (BA) enhances tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated cytotoxicity in T24 human bladder cancer cells. T24 cells were treated with the indicated concentrations of BA and TRAIL alone or in combination for 24 h. (A, B) After treatment, cell viability was assessed via 3′-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. (C) Morphological changes in the cells treated with BA and TRAIL alone or in combination were observed under an inverted microscope. (D, E) After 4′,6-diamidino-2-phenylindole (DAPI) staining, nuclear morphological changes were observed under a fluorescence microscope (D), and the frequency of cells with chromatin condensation and fragmentation was determined (E). (F, G) Flow cytometry was performed after propidium iodide (PI) staining. Representative histograms (F) and the frequency of cells in the sub-G1 phase (G) are shown. * p <0.05, ** p <0.01, and *** p <0.001 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3).

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: MTT Assay, Inverted Microscopy, Staining, Fluorescence, Microscopy, Flow Cytometry, Control

Combination treatment with BA and TRAIL increases reactive oxygen species (ROS) production and decreases ATP levels in T24 human bladder cancer cells. T24 cells were treated with BA and TRAIL alone or in combination and cultured for 30 min (A-C) or 24 h (D). (A, B) After treatment, the cells were stained with 2′,7′-dichlorofluorescein diacetate (DCF-DA) and analyzed via flow cytometry. Representative histograms (A) and the frequency of DCF-positive cells (B) are shown. (C) Representative fluorescence images of the cells stained with DCF-DA, indicating ROS production, were captured via fluorescence microscopy. (D) Intracellular ATP levels were measured using an ATP assay kit. * p <0.05 and ** p <0.01 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3).

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Combination treatment with BA and TRAIL increases reactive oxygen species (ROS) production and decreases ATP levels in T24 human bladder cancer cells. T24 cells were treated with BA and TRAIL alone or in combination and cultured for 30 min (A-C) or 24 h (D). (A, B) After treatment, the cells were stained with 2′,7′-dichlorofluorescein diacetate (DCF-DA) and analyzed via flow cytometry. Representative histograms (A) and the frequency of DCF-positive cells (B) are shown. (C) Representative fluorescence images of the cells stained with DCF-DA, indicating ROS production, were captured via fluorescence microscopy. (D) Intracellular ATP levels were measured using an ATP assay kit. * p <0.05 and ** p <0.01 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3).

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Cell Culture, Staining, Flow Cytometry, Fluorescence, Microscopy, ATP Assay, Control

$Combination treatment with BA and TRAIL increases mitochondrial damage and induces changes in the expression levels of Bcl-2 family proteins in T24 human bladder cancer cells. T24 cells were treated with BA and TRAIL alone or in combination and cultured for 24 h. (A, B) After treatment, the cells were stained with 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetramethylbenzimidazolyl carbocyanine iodide (JC-1) and analyzed via flow cytometry. Representative histograms (A) and the frequency of cells with JC-1 monomers (B), indicating mitochondrial membrane potential (MMP) loss, are shown. * p <0.05 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3). (C, D) Mitochondrial and cytosolic fractions were isolated from the cells (C), total protein was extracted (D), and immunoblotting was performed using antibodies against target proteins. Cytochrome c oxidase (COX IV) and β-actin were used as loading controls for the two fractions, respectively.$

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Combination treatment with BA and TRAIL increases mitochondrial damage and induces changes in the expression levels of Bcl-2 family proteins in T24 human bladder cancer cells. T24 cells were treated with BA and TRAIL alone or in combination and cultured for 24 h. (A, B) After treatment, the cells were stained with 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetramethylbenzimidazolyl carbocyanine iodide (JC-1) and analyzed via flow cytometry. Representative histograms (A) and the frequency of cells with JC-1 monomers (B), indicating mitochondrial membrane potential (MMP) loss, are shown. * p <0.05 vs. control cells; ### p <0.001 vs. BA-treated cells (n=3). (C, D) Mitochondrial and cytosolic fractions were isolated from the cells (C), total protein was extracted (D), and immunoblotting was performed using antibodies against target proteins. Cytochrome c oxidase (COX IV) and β-actin were used as loading controls for the two fractions, respectively.

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Expressing, Cell Culture, Staining, Flow Cytometry, Membrane, Control, Isolation, Western Blot

Combination treatment with BA and TRAIL activates the caspase-dependent extrinsic and intrinsic apoptotic pathways in T24 human bladder cancer cells. T24 cells were either directly co-treated with BA and TRAIL or pretreated with z-VAD-fmk for 1 h before co-treatment with BA and TRAIL and cultured for 24 h. (A) Total protein was extracted, and immunoblotting analysis was performed using antibodies against target proteins. (B) Caspase activity was examined using caspase assay kits. (C, D) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (C), and the frequency of cells with chromatin condensation and fragmentation was determined (D). (E, F) Flow cytometry was performed after PI staining. Representative histograms (E) and the frequency of cells in the sub-G1 phase (F) are shown. ** p <0.01 and *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Combination treatment with BA and TRAIL activates the caspase-dependent extrinsic and intrinsic apoptotic pathways in T24 human bladder cancer cells. T24 cells were either directly co-treated with BA and TRAIL or pretreated with z-VAD-fmk for 1 h before co-treatment with BA and TRAIL and cultured for 24 h. (A) Total protein was extracted, and immunoblotting analysis was performed using antibodies against target proteins. (B) Caspase activity was examined using caspase assay kits. (C, D) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (C), and the frequency of cells with chromatin condensation and fragmentation was determined (D). (E, F) Flow cytometry was performed after PI staining. Representative histograms (E) and the frequency of cells in the sub-G1 phase (F) are shown. ** p <0.01 and *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Cell Culture, Western Blot, Activity Assay, Caspase Assay, Staining, Fluorescence, Microscopy, Flow Cytometry, Control

Combination treatment with BA and TRAIL inhibits activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway in T24 human bladder cancer cells. T24 cells were either directly co-treated with BA and TRAIL or pretreated with LY294002 for 1 h before co-treatment with BA and TRAIL and cultured for 24 h. (A) Total cellular proteins were isolated from the cells, and phosphorylation levels of PI3K and Akt were determined via immunoblotting. (B, C) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (B), and the frequency of cells with chromatin condensation and fragmentation was determined (C). (D, E) Flow cytometry was performed after PI staining. Representative histograms (D) and the frequency of cells in the sub-G1 phase (E) are shown. (F) Cell viability was assessed via MTT assay. *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Combination treatment with BA and TRAIL inhibits activation of the phosphoinositide 3-kinase (PI3K)/Akt pathway in T24 human bladder cancer cells. T24 cells were either directly co-treated with BA and TRAIL or pretreated with LY294002 for 1 h before co-treatment with BA and TRAIL and cultured for 24 h. (A) Total cellular proteins were isolated from the cells, and phosphorylation levels of PI3K and Akt were determined via immunoblotting. (B, C) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (B), and the frequency of cells with chromatin condensation and fragmentation was determined (C). (D, E) Flow cytometry was performed after PI staining. Representative histograms (D) and the frequency of cells in the sub-G1 phase (E) are shown. (F) Cell viability was assessed via MTT assay. *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Activation Assay, Cell Culture, Isolation, Phospho-proteomics, Western Blot, Staining, Fluorescence, Microscopy, Flow Cytometry, MTT Assay, Control

Combination treatment with BA and TRAIL increases apoptosis in T24 human bladder cancer cells in an ROS-dependent manner. T24 cells were pretreated with N-acetyl-l-cysteine (NAC) 1 h before combination treatment with BA and TRAIL and cultured for 24 h. (A, B) Total protein was extracted and analyzed via immunoblotting using antibodies against target proteins. β-actin was used as a loading control. (C) Caspase-3 activity was measured using a caspase-3 assay kit. (D, E) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (D), and the frequency of cells with chromatin condensation and fragmentation was determined (E). (F, G) Flow cytometry was performed after PI staining. Representative histograms (F) and the frequency of cells in the sub-G1 phase (G) are shown. (H) Cell viability was assessed via MTT assay. *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Combination treatment with BA and TRAIL increases apoptosis in T24 human bladder cancer cells in an ROS-dependent manner. T24 cells were pretreated with N-acetyl-l-cysteine (NAC) 1 h before combination treatment with BA and TRAIL and cultured for 24 h. (A, B) Total protein was extracted and analyzed via immunoblotting using antibodies against target proteins. β-actin was used as a loading control. (C) Caspase-3 activity was measured using a caspase-3 assay kit. (D, E) After DAPI staining, nuclear morphological changes were observed under a fluorescence microscope (D), and the frequency of cells with chromatin condensation and fragmentation was determined (E). (F, G) Flow cytometry was performed after PI staining. Representative histograms (F) and the frequency of cells in the sub-G1 phase (G) are shown. (H) Cell viability was assessed via MTT assay. *** p <0.001 vs. control cells; ### p <0.001 vs. BA and TRAIL co-treated cells (n=3).

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Cell Culture, Western Blot, Control, Activity Assay, Caspase-3 Assay, Staining, Fluorescence, Microscopy, Flow Cytometry, MTT Assay

Schematic diagram of cytotoxicity induction in betulinic acid and TRAIL co-treated T24 human bladder cancer cells. TRAIL, tumor necrosis factor-related apoptosis-inducing ligand; PI3K, phosphoinositide 3-kinase; NAC, N-acetyl-l-cysteine; MMP, mitochondrial membrane potential; FADD, Fas-associated death domain; tBid, truncation of BH3-interacting domain death agonist; PARP, poly(ADP-ribose) polymerase.

Journal: Biomolecules & Therapeutics

Article Title: Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells

doi: 10.4062/biomolther.2026.035

Figure Lengend Snippet: Schematic diagram of cytotoxicity induction in betulinic acid and TRAIL co-treated T24 human bladder cancer cells. TRAIL, tumor necrosis factor-related apoptosis-inducing ligand; PI3K, phosphoinositide 3-kinase; NAC, N-acetyl-l-cysteine; MMP, mitochondrial membrane potential; FADD, Fas-associated death domain; tBid, truncation of BH3-interacting domain death agonist; PARP, poly(ADP-ribose) polymerase.

Article Snippet: T24 human bladder cancer cells obtained from the American Type Culture Collection (Manassas, VA, USA) were cultured as previously described ( Kim et al. , 2021 ).

Techniques: Membrane

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