647-V

Cat.No.: CSC-C0457

Species: Homo sapiens (Human)

Source: Bladder

Morphology: adherent epithelial-like cells growing in monolayers

Culture Properties: monolayer

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Cat.No.

CSC-C0457

Description

Established from a male patient with a primary urothelial bladder carcinoma (malignant, grade 2)

Species

Homo sapiens (Human)

Source

Bladder

Recommended Medium

85% DMEM + 15% h.i.FBS

Culture Properties

monolayer

Morphology

adherent epithelial-like cells growing in monolayers

Karyotype

Human flat-moded hyperdiploid/hypotriploid karyotype with 12% polyploidy - 52-60<3n>XX, -X/Y, -2, -4, -6, -9, -10, -12, -12, -14, -15, -16, -17, -18, +5mar, del(1)(p32), del(2)(q23)/add(2)(q2?), add(3)(q27), add(3)(q1?), i(5p), i(6p), i(7p)x2, add(8)(q24)

Disease

Bladder Carcinoma

Quality Control

Mycoplasma: negative in DAPI, microbiological culture, RNA hybridization, PCR assays
Immunology: cytokeratin +, cytokeratin-7 +, cytokeratin-8 +, cytokeratin-17 +, cytokeratin-18 +, cytokeratin-19 +, desmin -, endothel -, EpCAM +, GFAP -, neurofilament -,

Storage and Shipping

Frozen with 70% medium, 20% FBS, 10% DMSO at about 2 x 10^6 cells/ampoule; ship in dry ice; store in liquid nitrogen

Synonyms

647V; 647 V

Citation Guidance

If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

The 647-V cell line is a well-established human model system derived from a primary, moderately differentiated transitional cell carcinoma (urothelial carcinoma) of the bladder. Since its isolation in the 1970s, it has served as a fundamental in vitro and in vivo tool for elucidating the pathophysiology of bladder cancer and advancing therapeutic development. This epithelial line exhibits characteristic cobblestone morphology, expresses standard urothelial markers like cytokeratins, and critically, retains a wild-type p53 status. This genetic profile distinguishes it from other common bladder cancer lines (e.g., T24, which harbors a mutant p53) and makes it a particularly valuable model for studying p53-dependent pathways in drug response, DNA damage repair, and cell cycle regulation.

Its primary advantages lie in its reliability, relevance, and translational utility. First, its origin from a primary tumor (rather than a metastatic site) preserves biologically relevant traits of localized, invasive disease. Second, its stable and robust growth in culture ensures experimental reproducibility for high-throughput assays. Third, and most importantly, it is competently tumorigenic in immunocompromised mice, enabling seamless transition from cellular experiments to pre-clinical in vivo studies of tumor growth, metastasis, and therapy response.

Cytotoxicity of ²¹²Pb-labeled Anti-PTK7 Antibody in 2D Adherent and 3D Multicellular Bladder Cancer Models

PTK7 is overexpressed in various malignancies, including bladder cancer, and is therefore a viable therapeutic target. This study evaluated the preclinical efficacy of [²¹²Pb]Pb-TCMC-chOI-1, a ²¹²Pb-labeled antibody targeting PTK7, for targeted alpha-emitting radionuclide therapy in bladder cancer using 2D adherent cultures (clonogenic assay) and 3D multicellular spheroid models (spheroid growth inhibition).

[²¹²Pb]Pb-TCMC-chOI-1 treatment resulted in activity- and time-dependent cytotoxicity, with enhanced sensitivity observed in cell lines with higher PTK7 levels. In clonogenic assays, the activity concentration required for 50% growth reduction was 48-74 kBq/mL, corresponding to 22-51 bound and 9-16 internalized ²¹²Pb atoms per cell. In 3D models, similar therapeutic effects were observed despite significantly lower activities (values of approximately 1 and 30 kBq/mL for KU-19-19 and 647-V cells, respectively), suggesting a more pronounced cross-fire effect. Flow cytometry demonstrated treatment-induced DNA damage, cell cycle perturbations and cell death, with response patterns correlating with overall treatment sensitivity. RT-112 and KU-19-19 cells showed superior responses compared to 647-V and T-24 cells, consistent with their higher PTK7 expression.

Quantification of cell viability and DNA damage in KU-19-19 and 647-V cells after exposure to 100 kBq/mL [212Pb]Pb-TCMC-chOI-1 for 24 h. — Fig. 1. Cell viability, apoptosis, DNA damage, and mitotic analysis in KU-19-19 and 647-V cells following [²¹²Pb]Pb-TCMC-chOI-1 treatment (Lindland, Kim, and Asta Juzeniene. 2025).

Cytotoxicity of [212Pb]Pb-TCMC-chOI-1 in 3D multicellular models. — Fig. 2. Growth inhibition of KU-19-19 and 647-V spheroids treated with [²¹²Pb]Pb-TCMC-mAbs (Lindland, Kim, and Asta Juzeniene. 2025).

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For research use only. Not for any other purpose.