A new human diploid cell strain, TIG-1, for the research on cellular aging

Ohashi, Masataka; Aizawa, Shin-Ichi; Ooka, Hiroshi; Ohsawa, Tomonori; Kaji, Koichi; Kondo, Hiroshi; Kobayashi, Toshifumi; Noumura, Tetsuo; Matsuo, Mitsuyoshi; Mitsui, Youji; Murota, Sei‐itsu; Yamamoto, Kiyotaka; Itô, Hisashi; Shimada, Haruo; Utakoji, Tadashi

doi:10.1016/0531-5565(80)90083-2

Cited by 145 publications

(48 citation statements)

References 11 publications

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“…18,24 TIG-1 cells expressed high levels of vimentin, a fibroblastic marker, but their CADM1 level was negligible in comparison with cultured mouse mast cells ( Figure 3B), as is the case with NIH/3T3 fibroblasts. 12 NCI-H28, Meso-1, and Meso-1-CADM1-Hi cells were labeled with DiI, and then seeded onto TIG-1 cell monolayers.…”

Section: Involvement Of Cadm1 In Adhesion Between Cocultured Mpm and mentioning

confidence: 99%

Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium

Ito

Hagiyama

Mimura

et al. 2008

Laboratory Investigation

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Cell adhesion molecule 1 (CADM1), formerly referred to as SgIGSF, TSLC1, or Necl-2, has been characterized as a mast-cell adhesion molecule that mediates efficient interactions with mesothelial cells. Here, we examined whether CADM1 might be involved in the diffuse tumor growth over the pleural surface that characterizes malignant pleural mesothelioma (MPM). Immunohistochemical and western blot analyses revealed that 14 (25%) of 57 MPMs expressed the full-length form of CADM1 on the cell membrane, but non-neoplastic mesothelial cells did not express it at all. The majority of available MPM cell lines also expressed the full-length form of CADM1. We compared CADM1-positive and -negative MPM cells in culture within soft agar and in coculture on mesothelial or fibroblastic monolayers. Within soft agar, CADM1-negative MPM cells were capable of forming colonies, whereas CADM1-positive cells were not, suggesting that CADM1 is a potential tumor suppressor of MPM, consistent with the past characterization of this molecule in other types of tumors. However, in coculture on mesothelial cell monolayers lacking full-length CADM1, CADM1-positive MPM cells spread more widely and grew more quickly, whereas the CADM1-negative cells piled up. Transfection of the CADM1-negative cells with CADM1 cDNA caused them to behave like the CADM1-positive cells, with faster, more widespread growth. These phenotypic differences were not detectable in cocultures on lung fibroblastic monolayers, in which all MPM cells grew much more slowly than on mesothelial cells, irrespective of CADM1 positivity. CADM1 thus appears to mediate efficient adhesion and growth of MPM cells specifically on mesothelial cells, probably via trans-heterophilic binding, and thus may be involved in the manifestation of a considerable subset of MPMs as diffusely growing tumors disseminated over the pleural surface.

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Section: Involvement Of Cadm1 In Adhesion Between Cocultured Mpm and mentioning

confidence: 99%

Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium

Ito

Hagiyama

Mimura

et al. 2008

Laboratory Investigation

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“…I. J. Fidler (The University of Texas). Human lung fibroblast cell line TIG-1 14) was purchased from Japanese Cancer Research Resources Bank-Cell (Tokyo). Cells were maintained in Dulbecco's modified Eagle's medium supplemented with 10% fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

Annexin VII as a Novel Marker for Invasive Phenotype of Malignant Melanoma

Kataoka

Ito

Asada

et al. 2000

Japanese Journal of Cancer Research

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Both F10 and BL6 sublines of B16 mouse melanoma cells are metastatic after intravenous injection, but only BL6 cells are metastatic after subcutaneous injection. While examining the genetic difference between the two sublines, we found a marked reduction of annexin VII expression in BL6 cells. In addition, fusion cell clones of both sublines were as poorly metastatic as F10 cells after subcutaneous injection, and contained the annexin VII message as abundantly as F10 cells. Hence, we examined whether the annexin VII expression was correlated with the less malignant phenotype of clinical cases by immunohistochemistry. Immunoreactivities to anti-annexin VII antibody in melanoma cells were evaluated quantitatively by using skin mast cells as an internal positive control. Eighteen patients with malignant melanoma were divided into two groups: lymph node metastasis-negative and positive groups. The ratio of numbers of patients positive versus negative to the antibody was significantly larger in the former than in the latter group. These results not only indicated that annexin VII serves as a marker for less invasive phenotype of malignant melanoma, but also suggested a possible role of annexin VII in tumor suppression. Key words: B16 melanoma -Ca 2+ -binding protein -Fusion cells -ImmunohistochemistryAn increasing number of people are suffering from malignant melanoma in various areas of the world. The major cause of death in the patients with melanoma is tumor metastasis. Several approaches, including immunologic examination, 1-3) single strand conformation polymorphism (SSCP), 4,5) and serological tumor markers, [6][7][8] have been applied to evaluate the metastatic potentials of melanoma cells. Immunohistochemistry is one of the simplest and most commonly used methods. However, few probes have been identified that serve as prognostic markers of malignant melanoma in immunohistochemistry. To seek a novel and useful prognostic marker, we have examined a variety of sublines of B16 mouse melanoma cells, which possess distinct metastatic potentials.9) The BL6 subline is one of the most malignant and is metastatic after both intravenous and subcutaneous injection, whereas F10 cells are metastatic only after intravenous injection.10, 11) The F1 subline is a parent of F10 cells and is poorly metastatic even after intravenous injection. 12)Previously, we determined the genetic dominance in the metastatic phenotype between F10 and F1 cells. Fusion cell clones of both cells were as highly metastatic after intravenous injection as F10 cells. High metastatic phenotype appeared to dominate in crosses between F1 and F10 cells. 13) In the present study, we determined the genetic dominance in the metastatic phenotype between F10 and BL6 cells, and found that the low metastatic phenotype was dominant in their crosses. This indicated that F10-derived metastasis-suppressive activity dominated over the BL6-derived metastasis-promoting activity. It is logical that factors essential for metastasis-suppressive activity are expressed in F...

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“…Expression and Localization of α-SMA and Type IV Collagen in Cultured Lung Fibroblasts To investigate the role of α chains of type IV collagen in lung myofibroblasts in vitro (as we did in vivo), we studied the functional change of TIG-1-20 cells, a well-characterized cultured human lung fibroblast cell line, 16 with TGF-β1 stimulation or with the knockdown of α1(IV) and α2(IV) chains. Because TGF-β1 stimulation has been reported to induce α-SMA expression in fibroblasts as differentiation into myofibroblasts for 1 to 4 days, [19][20][21] we cultured the cells for 0 to 168 h (7 days) with TGF-β1 treatment to examine the effect of TGF-β1 on mRNA expression of α(IV) chains in TIG-1-20 cells at various time points.…”

Section: Deposition Of Type I Iii and Iv Collagens And α Chains Of mentioning

confidence: 99%

“…16) were provided by the Cell Resource Center for Biomedical Research, Institute of Development, Aging and Cancer, Tohoku University, and were purchased from the Health Science Research Resources Bank. TIG-1-20 cells were cultured in Dulbecco's modified Eagle's medium (DMEM; Wako Pure Chemical Industries, Osaka, Japan) supplemented with 10% fetal bovine serum (FBS), 50 μg/ml streptomycin, and 50 U/ml penicillin at 37°C under humidified 5% CO 2 / 95% air.…”

Section: Cell Culturementioning

confidence: 99%

Role of α1 and α2 chains of type IV collagen in early fibrotic lesions of idiopathic interstitial pneumonias and migration of lung fibroblasts

Urushiyama

Terasaki

Nagasaka

et al. 2015

Laboratory Investigation

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Early fibrotic lesions are thought to be the initial findings of fibrogenesis in idiopathic interstitial pneumonias, but little is known about their properties. Type IV collagen comprises six gene products, α1-α6, and although it is known as a major basement membrane component, its abnormal deposition is seen in fibrotic lesions of certain organs. We studied the expression of type I and III collagen and all α chains of type IV collagen in lung specimens from patients with usual interstitial pneumonia (UIP) or organizing pneumonia (OP) via immunohistochemistry. With cultured lung fibroblasts, we analyzed the expression and function of all α chains of type IV collagen via immunohistochemistry, western blotting, realtime quantitative PCR, and a Boyden chamber migration assay after the knockdown of α1 and α2 chains. Although we observed type I and III collagens in early fibrotic lesions of both UIP and OP, we found type IV collagen, especially α1 and α2 chains, in early fibrotic lesions of UIP but not OP. Fibroblasts enhanced the expression of α1 and α2 chains of type IV collagen after transforming growth factor-β1 stimulation. Small interfering RNA against α1 and α2 chains increased fibroblast migration, with upregulated phosphorylation of focal adhesion kinase (FAK), and adding medium containing fibroblast-produced α1 and α2 chains reduced the increased levels of fibroblast migration and phosphorylation of FAK. Fibroblasts in OP were positive for phosphorylated FAK but fibroblasts in UIP were not. These results suggest that fibroblasts in UIP with type IV collagen deposition, especially α1 and α2 chains, have less ability to migrate from early fibrotic lesions than fibroblasts in OP without type IV collagen deposition. Thus, type IV collagen deposition in early fibrotic lesions of UIP may be implicated in refractory pathophysiology including migration of lesion fibroblasts via a FAK pathway.

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A new human diploid cell strain, TIG-1, for the research on cellular aging

Cited by 145 publications

References 11 publications

Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium

Expression of cell adhesion molecule 1 in malignant pleural mesothelioma as a cause of efficient adhesion and growth on mesothelium

Annexin VII as a Novel Marker for Invasive Phenotype of Malignant Melanoma

Role of α1 and α2 chains of type IV collagen in early fibrotic lesions of idiopathic interstitial pneumonias and migration of lung fibroblasts

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