Morphological Characterization of Two Established Cell Lines, T24 and MGH-U1, Derived from Human Urinary Bladder Carcinoma

Kato, Takumi; Ishikawa, Kiyoshi; Nemoto, Ryosuke; Senoo, Akira; Amano, Yasuji

doi:10.1620/tjem.124.339

Cited by 25 publications

(13 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…RIG-I is also expressed in vascular endothelial cells stimulated with lipopolysaccharide (Imaizumi et al 2002), and porcine homologue of RIG-I, RNA helicase induced by virus (RHIV-1), is induced in macrophages infected with porcine reproductive and respiratory syndrome virus (Zhang et al 2000). In the present study, we have addressed the expression of RIG-I in T24 urinary bladder carcinoma cells, which has been used as a model of urothelium (Kato et al 1978;Byrne et al 1989;Shiono and Ike 1999). We also examined the expression of RIG-I in the bladder epithelium and carcinoma in vivo.…”

Section: Reverse Transcription-polymerase Chain Reactionmentioning

confidence: 92%

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Imaizumi

Yagihashi²,

Hatakeyama

et al. 2004

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Urinary bladder epithelial cells play an important role in the host defense against urinary tract infections. Interferon-γ (IFN-γ ) is a potent cytokine that regulates immune responses by inducing multiple genes in many types of cells including urinary bladder epithelial cells. Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH-box family, which is involved in various reactions related to RNA metabolism, and is induced in leukemic cells by retinoic acid or in endothelial cells by lipopolysaccharide. We have studied the expression of RIG-I in T24 cells, a cell line derived from human urinary bladder epithelial carcinoma cells. IFN-γ stimulated T24 cells to express RIG-I mRNA and protein in concentration-and time-dependent manners. Immunohistochemical analysis revealed the expression of RIG-I in the urinary bladder epithelium from a patient with chronic urinary tract infection and in a bladder epithelial carcinoma. We conclude that RIG-I may play some role in inflammatory reactions in the urinary tract epithelium.RIG-I; IFN-γ ; T24 cells; urinary bladder epithelial cells

show abstract

Section: Reverse Transcription-polymerase Chain Reactionmentioning

confidence: 92%

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Imaizumi

Yagihashi²,

Hatakeyama

et al. 2004

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

show abstract

“…This cell line had a heterogeneous chromosome constitution with both diploid and tetraploid subpopulations which became predominantly tetraploid (80% of the cells) after prolonged culture (Hastings and Franks, 1981). The EJ line has been designated MGH-U1 by Kato et al (1977), although karyotypic analysis of MGH-U1 showed only the tetraploid population (Kato et al, 1978 Pasteur pipette and growing each separately in Microwell plates (Flow Laboratories, Irvine, Scotland). Each clone has been maintained in longterm culture, although the results presented in this study were obtained using cells earlier than the 20th passage.…”

Section: Materials and Methods Origin Of Ej Cell Line And Clonesmentioning

confidence: 99%

Cellular heterogeneity in a tissue culture cell line derived from a human bladder carcinoma

Hastings¹,

Franks²

1983

Br J Cancer

View full text Add to dashboard Cite

Summary To study heterogeneity in a cell line derived from a human bladder carcinoma (EJ), 7 clones were isolated at low passage and examined for differences in culture behaviour, ability to grow in agar and tumorigenicity in nude mice. The parent EJ line had several distinct chromosome populations (both diploid and tetraploid), grew in agar and produced tumours in nude mice. Three of the clones had pseudodiploid modes and 4 had either hypo-or hypertetraploid modes. The 7 clones had 5 marker chromosomes in common but the combination of other marker chromosomes made each clone unique. No Differences were also found in the packing density of the cloned cells and in the cell size. All 7 clones grew in agar but heterogeneity was seen between the clones as shown by widely varying colony-forming efficiencies (0.5-13%). One clone had a high colony-forming ability in agar but failed to produce tumours in nude mice. The other clones were tumorigenic regardless of colony-forming efficiency in agar. Specific chromosome abnormalities were found to be associated with growth in agar and tumorigenicity but not with the growth pattern or the rate of movement of the cloned cells in culture.

show abstract

“…The T24 human urinary bladder carcinoma cell line originated from an 81-year-old patient by Bubeník et al (1973) and was characterized by Marshall et al (1977), Kato et al (1978), Capon et al (1983), andO'Toole et al (1983). Ultrastructural studies reveal a number of features shared by a wide variety of tumors, including high nuclear-to-protoplasmic ratio, a loose chromatin texture, and poor differentiation (Kato et al, 1978;Srigley et al, 1988).…”

Section: Cell Linementioning

confidence: 99%

“…Ultrastructural studies reveal a number of features shared by a wide variety of tumors, including high nuclear-to-protoplasmic ratio, a loose chromatin texture, and poor differentiation (Kato et al, 1978;Srigley et al, 1988). Karyotyping studies reveal these cells are hypertriploid to hypertetraploid.…”

Section: Cell Linementioning

confidence: 99%

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Gilloteaux¹,

Jamison²,

Arnold³

et al. 2005

Anat. Rec.

View full text Add to dashboard Cite

Feulgen and actin-phalloidin staining as well as gel electrophoresis have been employed in conjunction with cell ultrastructure to describe the effects of 1-, 2-, and 4-hr ascorbate (VC), menadione (VK 3 ), and ascorbate:menadione (VC:VK 3 ) treatments on the T24 human bladder carcinoma cell line. T24 cells exposed to VC alone display blebs and other superficial membrane defects related to membrane alterations and to superficial cytoskeleton changes. VK 3 treatment damages the cell nucleus and organelles, leads to the redistribution of the organelles in the perikaryon as a consequence of cytoskeletal damage, and results in cytoplasmic self-excisions. After VC:VK 3 treatment, the cells show exaggerated alterations characteristic of each vitamin treatment alone, including damaged mitochondria, self-excision of organelle-free pieces of cytoplasm, and extrusion of the perikaryon containing a nucleus surrounded by the damaged organelles. The nuclear envelope appears intact and contains chromatin that decondenses and dissipates. During the cellular demise that concludes with apparent karyolysis, the cells significantly decrease their size and alter their shape. However, the cisterns of rough endoplasmic reticulum are undamaged, but may become dilated. Since the cellular phenomena leading to cell death differ morphologically from apoptosis and necrosis, but entail selfcutting without nuclear bodies, this new form of cell death was called autoschizis. In addition, gel electrophoresis and Feulgen staining demonstrate that autoschizis is accompanied by random DNA degeneration.

show abstract

Morphological Characterization of Two Established Cell Lines, T24 and MGH-U1, Derived from Human Urinary Bladder Carcinoma

Cited by 25 publications

References 12 publications

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Upregulation of Retinoic Acid-Inducible Gene-I in T24 Urinary Bladder Carcinoma Cells Stimulated with Interferon-.GAMMA.

Cellular heterogeneity in a tissue culture cell line derived from a human bladder carcinoma

Morphology and DNA degeneration during autoschizic cell death in bladder carcinoma T24 cells induced by ascorbate and menadione treatment

Contact Info

Product

Resources

About