Establishment of human tumor cell line (Ueda-1) derived from squamous cell carcinoma of the floor of the mouth.

Miyauchi, Shunsuke; Moroyama, Takamasa; Sakamoto, Tomoji; Okamoto, Tomoyoshi; Takada, Kazuaki

doi:10.5794/jjoms.31.1347

Cited by 16 publications

(9 citation statements)

References 5 publications

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“…Human oral epithelial cell lines HSC-2 (30), HO-1-u-1 (31), and KB (32), established from squamous cell carcinoma, were obtained from the Cancer Cell Repository, Institute of Development, Aging and Cancer, Tohoku University (Sendai, Japan). A human colon adenocarcinoma cell line SW620 (CCL-227) and a human cervical epitheloid carcinoma HeLa (JCRB9004) were obtained from the American Type Culture Collection (Rockville, MD) and Health Science Research Resources Bank (Osaka, Japan), respectively.…”

Section: Cells and Cell Culturementioning

confidence: 99%

Proinflammatory Cytokines Induce Proteinase 3 as Membrane-Bound and Secretory Forms in Human Oral Epithelial Cells and Antibodies to Proteinase 3 Activate the Cells through Protease-Activated Receptor-2

Uehara¹,

Sugawara

Sasano

et al. 2004

The Journal of Immunology

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Anti-neutrophil cytoplasmic Abs targeting proteinase 3 (PR3) have been detected in relation to a wide range of inflammatory conditions such as periodontitis, and interaction of anti-PR3 Abs with endothelial and epithelial cells provokes cell activation, although the underlying mechanism has been unclear. The present study showed that human oral epithelial cells expressed PR3 mRNA after treatment with proinflammatory cytokines such as IL-1alpha, TNF-alpha, IFN-alpha, IFN-beta, and IFN-gamma. A 29-kDa PR3 was expressed on the cell surface and released into culture supernatants by the cells upon stimulation with these cytokines. The membrane and supernatant fractions of oral epithelial cells exhibited enzymatic activity, which was inhibited by serine proteinase inhibitors, but not by a cysteine proteinase inhibitor or secretory leukocyte protease inhibitor. Addition of anti-PR3 Abs to cytokine-primed oral epithelial cells in culture induced remarkable secretion of IL-8 and monocyte chemoattractant protein 1 and aggregation of PR3 on the cells. RNA interference targeted to protease-activated receptor-2 mRNA and intracellular Ca2+ mobilization assays revealed that anti-PR3 Abs activated the epithelial cells through protease-activated receptor-2, a family of G protein-coupled receptors. The anti-PR3 Ab-mediated cell activation was completely abolished by RNA interference targeted to PR3 mRNA and by inhibition of phospholipase C and NF-kappaB. Immunohistochemistry showed that inflamed oral epithelium actually expresses PR3 protein. These results suggest that oral epithelial cells express functional PR3 in the inflamed sites and respond to anti-PR3 Abs detected in diseased sera, and that these mechanisms may actively participate in the inflammatory process, including periodontitis.

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Section: Cells and Cell Culturementioning

confidence: 99%

Proinflammatory Cytokines Induce Proteinase 3 as Membrane-Bound and Secretory Forms in Human Oral Epithelial Cells and Antibodies to Proteinase 3 Activate the Cells through Protease-Activated Receptor-2

Uehara¹,

Sugawara

Sasano

et al. 2004

The Journal of Immunology

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“…Before stimulation of HGFs, the culture medium was changed to MEMα containing 10% FBS and no antibiotics. The human oral epithelial cell lines HSC‐2 (32) and HO‐1‐u‐1 (33), originally established from squamous cell carcinoma, were obtained from the Cancer Cell Repository, Institute of Development, Aging and Cancer (Tohoku University, Sendai, Japan). These cell lines were grown in MEMα containing 10% FBS, 50 U ml −1 of penicillin, and 50 μ g ml −1 of streptomycin at 37°C in an atmosphere containing 5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Suppressive effect of the antimicrobial peptide LL‐37 on expression of IL‐6, IL‐8 and CXCL10 induced by Porphyromonas gingivalis cells and extracts in human gingival fibroblasts

Inomata

Into

Murakami

2010

European J Oral Sciences

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Porphyromonas gingivalis is a major periodontogenic bacterium and possesses immunostimulatory components, such as lipopolysaccharides (LPS) and fimbriae. The host antimicrobial peptide, LL-37, suppresses proinflammatory responses of immune cells but its effect on human gingival fibroblasts (HGFs) is not known. In this study, we assessed the effect of LL-37 on the proinflammatory responses of HGFs stimulated with P. gingivalis cells and their components. Live P. gingivalis cells did not induce proinflammatory responses of HGFs, and LL-37 did not alter these responses. However, LL-37 was able to suppress the killed P. gingivalis cell-induced secretion of interleukin (IL)-6 and IL-8. LL-37 also suppressed the expression of IL6, IL8, and CXCL10 genes that was induced by P. gingivalis components, including phenol-water extracts, lipid A, and fimbriae, and the induction of phosphorylation of p38 and extracellular signal-regulated kinase (ERK) by P. gingivalis lipopolysaccharide (LPS). CAMP was found to be expressed in oral epithelial cells but not in HGFs, despite stimulation with P. gingivalis components. Therefore, LL-37 can exert a suppressive effect on P. gingivalis-induced proinflammatory responses of HGFs in a paracrine manner, suggesting that excess inflammatory responses to P. gingivalis in the gingival tissue are suppressed by LL-37 in vivo.

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“…The human oral epithelial cell lines HSC‐2 (Momose et al ., 1989), HO‐1‐u‐1 (Miyauchi et al ., 1985) and KB (Eagle, 1955), established from squamous cell carcinoma, were obtained from the Cancer Cell Repository, Institute of Development, Aging and Cancer, Tohoku University (HSC‐2 and HO‐1‐u‐1; Sendai, Japan) and from the Health Science Research Resources Bank (KB; Tokyo, Japan). HSC‐2 and HO‐1‐u‐1 were grown in RPMI 1640 medium (Nissui Seiyaku, Tokyo, Japan) with 10% heat‐inactivated fetal calf serum (FCS; Life Technologies, Grand Island, NY, USA) and KB was grown in alpha‐modified minimum essential medium (α‐MEM; Flow Laboratories, McLean, VA, USA) with 10% FCS with a medium change every 3 days.…”

Section: Methodsmentioning

confidence: 99%

Chemically synthesized pathogen-associated molecular patterns increase the expression of peptidoglycan recognition proteins via toll-like receptors, NOD1 and NOD2 in human oral epithelial cells

Uehara

Sugawara

Kurata

et al. 2005

Cellular Microbiology

114

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Establishment of human tumor cell line (Ueda-1) derived from squamous cell carcinoma of the floor of the mouth.

Cited by 16 publications

References 5 publications

Proinflammatory Cytokines Induce Proteinase 3 as Membrane-Bound and Secretory Forms in Human Oral Epithelial Cells and Antibodies to Proteinase 3 Activate the Cells through Protease-Activated Receptor-2

Proinflammatory Cytokines Induce Proteinase 3 as Membrane-Bound and Secretory Forms in Human Oral Epithelial Cells and Antibodies to Proteinase 3 Activate the Cells through Protease-Activated Receptor-2

Suppressive effect of the antimicrobial peptide LL‐37 on expression of IL‐6, IL‐8 and CXCL10 induced by Porphyromonas gingivalis cells and extracts in human gingival fibroblasts

Chemically synthesized pathogen-associated molecular patterns increase the expression of peptidoglycan recognition proteins via toll-like receptors, NOD1 and NOD2 in human oral epithelial cells

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