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human bladder transitional cell carcinoma cell lines  (ATCC)


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    ATCC human bladder transitional cell carcinoma cell lines
    Human Bladder Transitional Cell Carcinoma Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 344 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+bladder+transitional+cell+carcinoma+cell+lines/T-24%3B+Bladder+Cancer%3B+Human/pmc12170997-23-0-13
    Average 96 stars, based on 344 article reviews
    human bladder transitional cell carcinoma cell lines - by Bioz Stars, 2026-09
    96/100 stars

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    Multiple Displacement Amplification:

    Article Title: Suppression of human tumor cell proliferation by Smurf2-induced senescence.
    Article Snippet: Cellular Physiology Suppression of Human Tumor Cell Proliferation by Smurf2-Induced Senescence HONG ZHANG,* YUCHIN TENG, YAHUI KONG, PAUL E. KOWALSKI, AND STANLEY N. COHEN** Department of Cell Biology, University of Massachusetts Medical School, Worcester, Massachusetts Department of Genetics, Stanford University School of Medicine, Stanford, California Department of Medicine, Stanford University School of Medicine, Stanford, California

    Cell Culture:

    Article Title: MAFG-AS1/MAFG positive feedback loop contributes to cisplatin resistance in bladder urothelial carcinoma through antagonistic ferroptosis.
    Article Snippet: Though promoting ferroptosis can reduce cisplatin resistance in tumor cells, ferroptosis and cisplatin resistance in bladder urothelial carcinoma (BUC) following long non-coding RNAs (lncRNAs) is largely unknown.. Here, we found the highly expressed lncRNA MAF transcription factor G antisense RNA 1 (MAFG-AS1) in BUC, and its inhibition increased the sensitivity of BUC cells to cisplatin by promoting ferroptosis.. Mechanically, binding to iron chaperone poly(rC)-binding protein 2 (PCBP2) facilitated the recruitments of MAFG-AS1 to deubiquitinase ubiquitin carboxyl-terminal hydrolase isozyme L5 (UCHL5), thus stabilizing PCBP2 protein itself.

    Modification:

    Article Title: MAFG-AS1/MAFG positive feedback loop contributes to cisplatin resistance in bladder urothelial carcinoma through antagonistic ferroptosis.
    Article Snippet: Though promoting ferroptosis can reduce cisplatin resistance in tumor cells, ferroptosis and cisplatin resistance in bladder urothelial carcinoma (BUC) following long non-coding RNAs (lncRNAs) is largely unknown.. Here, we found the highly expressed lncRNA MAF transcription factor G antisense RNA 1 (MAFG-AS1) in BUC, and its inhibition increased the sensitivity of BUC cells to cisplatin by promoting ferroptosis.. Mechanically, binding to iron chaperone poly(rC)-binding protein 2 (PCBP2) facilitated the recruitments of MAFG-AS1 to deubiquitinase ubiquitin carboxyl-terminal hydrolase isozyme L5 (UCHL5), thus stabilizing PCBP2 protein itself.



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    ATCC human bladder transitional cell carcinoma tcc cell lines j82
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    ATCC human urinary bladder transitional cell carcinoma tcc cell lines j82
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    ATCC human urinary bladder transitional cell carcinoma cell lines j82
    Figure 1. HME’s cytotoxic effect on human bladder TCC cell lines. (A) HME induces stronger cytotoxicity than cisplatin against human bladder TCC cells. Human bladder TCC cell lines <t>J82,</t> T24, and TCCSUP were treated with HME or cisplatin (0~200 µM) for 48 h, followed by cell viability determination using MTS assay. (B) HME impairs the colony-forming capacity of human bladder TCC cells. The levels of clonogenicity of HME-treated J82, T24, and TCCSUP cells were determined as described in Section 4. ***: p < 0.001. (C) Higher cytotoxic effect of HME than hispolon on TCCSUP cells while comparable cytotoxicity of these two drugs against J82 and T24 cells. J82, T24, and TCCSUP were treated with HME or hispolon (0~200 µM) for 48 h, followed by cell viability determination using MTS assay.
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    European Collection of Authenticated Cell Cultures human urinary bladder transitional cell carcinoma cell line um-uc-1
    circNCOR1 inhibits LN metastasis of bladder cancer by inhibiting the TGFβ–SMAD signaling pathway. A – C, Representative images ( A ) and quantification of the tube formation ( B ) and Transwell migration ( C ) by HLECs cocultured with UM-UC-3 cells. Scale bars, 100 μm. D, The popliteal LN metastatic rate in the nude mice ( n = 12 per group). E and F, Bioluminescence ( E ) and LN volume ( F ) of popliteal LN metastasis in the nude mice ( n = 12 per group). G, Luciferase activity of the SMAD7 promoter in indicated UM-UC-3 cells. H, qRT-PCR analysis of SMAD7 expression in indicated UM-UC-3 cells. I and J, Western blotting of SMAD7 expression in indicated UM-UC-3 ( I ) and <t>T24</t> ( J ) cells. The statistical difference was assessed by the two-tailed Student t test in B , C , E , and F , and the χ 2 test in D ; and one-way ANOVA followed by Dunnett tests in G and H . Error bars show the SD from three independent experiments. **, P < 0.01.
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    Pro-cell Co Ltd t24 human bladder transitional cell carcinoma cell line
    Human antigen R (HuR) promotes the proliferation of <t>T24</t> cells. Compared to the control group, after 48 h, cell viability was significantly increased in the HuR overexpression group and significantly decreased in the HuR knockdown group (F=1929.061, P<0.01). *, P<0.05.
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    Figure 1. HME’s cytotoxic effect on human bladder TCC cell lines. (A) HME induces stronger cytotoxicity than cisplatin against human bladder TCC cells. Human bladder TCC cell lines J82, T24, and TCCSUP were treated with HME or cisplatin (0~200 µM) for 48 h, followed by cell viability determination using MTS assay. (B) HME impairs the colony-forming capacity of human bladder TCC cells. The levels of clonogenicity of HME-treated J82, T24, and TCCSUP cells were determined as described in Section 4. ***: p < 0.001. (C) Higher cytotoxic effect of HME than hispolon on TCCSUP cells while comparable cytotoxicity of these two drugs against J82 and T24 cells. J82, T24, and TCCSUP were treated with HME or hispolon (0~200 µM) for 48 h, followed by cell viability determination using MTS assay.

    Journal: International journal of molecular sciences

    Article Title: Hispolon Methyl Ether, a Hispolon Analog, Suppresses the SRC/STAT3/Survivin Signaling Axis to Induce Cytotoxicity in Human Urinary Bladder Transitional Carcinoma Cell Lines.

    doi: 10.3390/ijms24010138

    Figure Lengend Snippet: Figure 1. HME’s cytotoxic effect on human bladder TCC cell lines. (A) HME induces stronger cytotoxicity than cisplatin against human bladder TCC cells. Human bladder TCC cell lines J82, T24, and TCCSUP were treated with HME or cisplatin (0~200 µM) for 48 h, followed by cell viability determination using MTS assay. (B) HME impairs the colony-forming capacity of human bladder TCC cells. The levels of clonogenicity of HME-treated J82, T24, and TCCSUP cells were determined as described in Section 4. ***: p < 0.001. (C) Higher cytotoxic effect of HME than hispolon on TCCSUP cells while comparable cytotoxicity of these two drugs against J82 and T24 cells. J82, T24, and TCCSUP were treated with HME or hispolon (0~200 µM) for 48 h, followed by cell viability determination using MTS assay.

    Article Snippet: Human urinary bladder transitional cell carcinoma cell lines J82 (ATCC HTB-1TM) and TCCSUP (ATCC HTB-5TM) were both cultured in Eagle’s Minimum Essential Medium, while the T24 cell line (ATCC HTB-4TM) in McCoy’s 5a medium in accordance with the recommendation of the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: MTS Assay

    Figure 2. HME’s proapoptotic effect on human bladder TCC cell lines. (A) Induction of PARP cleavage by HME. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting to evaluate the levels of PARP cleavage. The levels of glyceraldehyde- 3-phosphate dehydrogenase (GAPDH) were used as a control for equal loading. c-PARP: cleaved PARP. (B) Increase of annexin V-positive (apoptotic) cell population by HME. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by flow cytometry-based annexin V/propidium iodide (PI) dual staining as described in Section 4. ***: p < 0.001.

    Journal: International journal of molecular sciences

    Article Title: Hispolon Methyl Ether, a Hispolon Analog, Suppresses the SRC/STAT3/Survivin Signaling Axis to Induce Cytotoxicity in Human Urinary Bladder Transitional Carcinoma Cell Lines.

    doi: 10.3390/ijms24010138

    Figure Lengend Snippet: Figure 2. HME’s proapoptotic effect on human bladder TCC cell lines. (A) Induction of PARP cleavage by HME. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting to evaluate the levels of PARP cleavage. The levels of glyceraldehyde- 3-phosphate dehydrogenase (GAPDH) were used as a control for equal loading. c-PARP: cleaved PARP. (B) Increase of annexin V-positive (apoptotic) cell population by HME. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by flow cytometry-based annexin V/propidium iodide (PI) dual staining as described in Section 4. ***: p < 0.001.

    Article Snippet: Human urinary bladder transitional cell carcinoma cell lines J82 (ATCC HTB-1TM) and TCCSUP (ATCC HTB-5TM) were both cultured in Eagle’s Minimum Essential Medium, while the T24 cell line (ATCC HTB-4TM) in McCoy’s 5a medium in accordance with the recommendation of the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: Western Blot, Control, Cytometry, Staining

    Figure 5. HME inhibits SRC to suppress the STAT3/survivin signaling axis. (A) HME inhibits SRC activation in all human bladder TCC cell lines examined. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting for the levels of tyrosine 1007/1008- phosphorylated JAK2 (p-JAK2), total JAK2, tyrosine 416-phosphorylated SRC (p-SRC), total SRC, and GAPDH (loading control). (B) Ectopic expression of v-src, a dominant-active SRC, rescues both p-STAT3 and survivin levels from HME-mediated suppression but also attenuates HME-induced PARP cleavage. TCCSUP stable clones of HA-v-src and the respective vector control were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting to evaluate the levels of HA, p-STAT3, total STAT3, survivin, c-PARP, and GAPDH (loading control). (C) v-src overexpression antagonizes the proapoptotic and cytotoxic effect of HME. TCCSUP stable clones of HA-v-src and the respective vector control were treated with HME (0, 30, 60 µM) for 24 h, followed by annexin V/PI dual staining assay (left) and clonogenicity assay (right) to examine the HME-induced apoptosis and cytotoxicity, respectively. *: p < 0.05; ***: p < 0.001.

    Journal: International journal of molecular sciences

    Article Title: Hispolon Methyl Ether, a Hispolon Analog, Suppresses the SRC/STAT3/Survivin Signaling Axis to Induce Cytotoxicity in Human Urinary Bladder Transitional Carcinoma Cell Lines.

    doi: 10.3390/ijms24010138

    Figure Lengend Snippet: Figure 5. HME inhibits SRC to suppress the STAT3/survivin signaling axis. (A) HME inhibits SRC activation in all human bladder TCC cell lines examined. J82, T24, and TCCSUP cells were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting for the levels of tyrosine 1007/1008- phosphorylated JAK2 (p-JAK2), total JAK2, tyrosine 416-phosphorylated SRC (p-SRC), total SRC, and GAPDH (loading control). (B) Ectopic expression of v-src, a dominant-active SRC, rescues both p-STAT3 and survivin levels from HME-mediated suppression but also attenuates HME-induced PARP cleavage. TCCSUP stable clones of HA-v-src and the respective vector control were treated with HME (0, 30, 60 µM) for 24 h, followed by immunoblotting to evaluate the levels of HA, p-STAT3, total STAT3, survivin, c-PARP, and GAPDH (loading control). (C) v-src overexpression antagonizes the proapoptotic and cytotoxic effect of HME. TCCSUP stable clones of HA-v-src and the respective vector control were treated with HME (0, 30, 60 µM) for 24 h, followed by annexin V/PI dual staining assay (left) and clonogenicity assay (right) to examine the HME-induced apoptosis and cytotoxicity, respectively. *: p < 0.05; ***: p < 0.001.

    Article Snippet: Human urinary bladder transitional cell carcinoma cell lines J82 (ATCC HTB-1TM) and TCCSUP (ATCC HTB-5TM) were both cultured in Eagle’s Minimum Essential Medium, while the T24 cell line (ATCC HTB-4TM) in McCoy’s 5a medium in accordance with the recommendation of the American Type Culture Collection (ATCC) (Manassas, VA, USA).

    Techniques: Activation Assay, Western Blot, Control, Expressing, Clone Assay, Plasmid Preparation, Over Expression, Staining

    circNCOR1 inhibits LN metastasis of bladder cancer by inhibiting the TGFβ–SMAD signaling pathway. A – C, Representative images ( A ) and quantification of the tube formation ( B ) and Transwell migration ( C ) by HLECs cocultured with UM-UC-3 cells. Scale bars, 100 μm. D, The popliteal LN metastatic rate in the nude mice ( n = 12 per group). E and F, Bioluminescence ( E ) and LN volume ( F ) of popliteal LN metastasis in the nude mice ( n = 12 per group). G, Luciferase activity of the SMAD7 promoter in indicated UM-UC-3 cells. H, qRT-PCR analysis of SMAD7 expression in indicated UM-UC-3 cells. I and J, Western blotting of SMAD7 expression in indicated UM-UC-3 ( I ) and T24 ( J ) cells. The statistical difference was assessed by the two-tailed Student t test in B , C , E , and F , and the χ 2 test in D ; and one-way ANOVA followed by Dunnett tests in G and H . Error bars show the SD from three independent experiments. **, P < 0.01.

    Journal: Cancer Research

    Article Title: Aberrant Nuclear Export of circNCOR1 Underlies SMAD7-Mediated Lymph Node Metastasis of Bladder Cancer

    doi: 10.1158/0008-5472.CAN-21-4349

    Figure Lengend Snippet: circNCOR1 inhibits LN metastasis of bladder cancer by inhibiting the TGFβ–SMAD signaling pathway. A – C, Representative images ( A ) and quantification of the tube formation ( B ) and Transwell migration ( C ) by HLECs cocultured with UM-UC-3 cells. Scale bars, 100 μm. D, The popliteal LN metastatic rate in the nude mice ( n = 12 per group). E and F, Bioluminescence ( E ) and LN volume ( F ) of popliteal LN metastasis in the nude mice ( n = 12 per group). G, Luciferase activity of the SMAD7 promoter in indicated UM-UC-3 cells. H, qRT-PCR analysis of SMAD7 expression in indicated UM-UC-3 cells. I and J, Western blotting of SMAD7 expression in indicated UM-UC-3 ( I ) and T24 ( J ) cells. The statistical difference was assessed by the two-tailed Student t test in B , C , E , and F , and the χ 2 test in D ; and one-way ANOVA followed by Dunnett tests in G and H . Error bars show the SD from three independent experiments. **, P < 0.01.

    Article Snippet: The human urinary bladder transitional cell carcinoma cell lines T24 (RRID: CVCL_0554), UM-UC-3 (RRID: CVCL_1783) were purchased from ATCC, RT112 (RRID: CVCL_1670) was purchased from German Collection of Microorganisms and Cell Cultures GmbH (DSMZ) and UM-UC-1 (RRID: CVCL_2743) was purchased from European Collection of Authenticated Cell Cultures (ECACC).

    Techniques: Migration, Luciferase, Activity Assay, Quantitative RT-PCR, Expressing, Western Blot, Two Tailed Test

    Human antigen R (HuR) promotes the proliferation of T24 cells. Compared to the control group, after 48 h, cell viability was significantly increased in the HuR overexpression group and significantly decreased in the HuR knockdown group (F=1929.061, P<0.01). *, P<0.05.

    Journal: Translational Andrology and Urology

    Article Title: The effects of modified RNA-binding proteins HuR on the biological behavior of the bladder cancer T24 cell line

    doi: 10.21037/tau-22-123

    Figure Lengend Snippet: Human antigen R (HuR) promotes the proliferation of T24 cells. Compared to the control group, after 48 h, cell viability was significantly increased in the HuR overexpression group and significantly decreased in the HuR knockdown group (F=1929.061, P<0.01). *, P<0.05.

    Article Snippet: Experimental materials The T24 human bladder transitional cell carcinoma cell line was purchased from Procell Co., Ltd., and mycoplasma testing was conducted for all cells.

    Techniques: Control, Over Expression, Knockdown

    Human antigen R (HuR) promotes the migration of T24 cells. Compared to the control group, the number of migrated cells of HuR overexpression group was significantly increased and significantly decreased in the HuR knockdown group (F=145.982, P<0.01, all the photos magnified at ×400; all the cells were stained by crystal violet staining). *, P<0.05. (A) Control group; (B) HuR overexpression group; (C) HuR knockdown group; (D) the number of cell migrations of each group.

    Journal: Translational Andrology and Urology

    Article Title: The effects of modified RNA-binding proteins HuR on the biological behavior of the bladder cancer T24 cell line

    doi: 10.21037/tau-22-123

    Figure Lengend Snippet: Human antigen R (HuR) promotes the migration of T24 cells. Compared to the control group, the number of migrated cells of HuR overexpression group was significantly increased and significantly decreased in the HuR knockdown group (F=145.982, P<0.01, all the photos magnified at ×400; all the cells were stained by crystal violet staining). *, P<0.05. (A) Control group; (B) HuR overexpression group; (C) HuR knockdown group; (D) the number of cell migrations of each group.

    Article Snippet: Experimental materials The T24 human bladder transitional cell carcinoma cell line was purchased from Procell Co., Ltd., and mycoplasma testing was conducted for all cells.

    Techniques: Migration, Control, Over Expression, Knockdown, Staining

    Human antigen R (HuR) inhibits T24 cell apoptosis. Compared to the control group, the apoptotic rate was significantly decreased in the HuR overexpression group and significantly increased in the knockdown group (F=665.452, P<0.01). *, P<0.05. (A) Control group; (B) HuR overexpression group; (C) HuR knockdown group; (D) each group apoptosis rate of T24 cell.

    Journal: Translational Andrology and Urology

    Article Title: The effects of modified RNA-binding proteins HuR on the biological behavior of the bladder cancer T24 cell line

    doi: 10.21037/tau-22-123

    Figure Lengend Snippet: Human antigen R (HuR) inhibits T24 cell apoptosis. Compared to the control group, the apoptotic rate was significantly decreased in the HuR overexpression group and significantly increased in the knockdown group (F=665.452, P<0.01). *, P<0.05. (A) Control group; (B) HuR overexpression group; (C) HuR knockdown group; (D) each group apoptosis rate of T24 cell.

    Article Snippet: Experimental materials The T24 human bladder transitional cell carcinoma cell line was purchased from Procell Co., Ltd., and mycoplasma testing was conducted for all cells.

    Techniques: Control, Over Expression, Knockdown