• 제목/요약/키워드: oral cell

검색결과 2,610건 처리시간 0.034초

방사선조사가 사람 정상 구강각화 세포의 세포주기, 세포사 및 수종 단백질의 발현에 미치는 영향 (Effect of irradiation on cell cycle, cell death and expression of its related proteins in normal human oral keratinocytes)

  • 강미애;허민석;이삼선;오성욱;이설미;전인성;최순철;박태원
    • Imaging Science in Dentistry
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    • 제33권3호
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    • pp.143-149
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    • 2003
  • Purpose: To investigate the radiosensitivity of the normal human oral keratinocytes (NHOK), and the effect of irradiation on cell cycle and protein expression. Materials and Methods: To evaluate the radiosensitivity of NHOK, the number of colonies and cells were counted after irradiation and the SF2 (survival fraction at 2Gy) value, and the cell survival curve fitted on a linear-quadratic model were obtained. LDH analysis was carried out to evaluate the necrosis of NHOK at 1, 2, 3, and 4 days after 2, 10, and 20 Gy irradiation. Cell cycle arrest and the induction of apoptosis were analyzed using flow cytometry at 1, 2, 3, and 4 days after 2, 10, and 200y irradiation. Finally, proteins related cell cycle arrest and apoptosis were analysed by Western blot. Results: The number of survived cell was significantly decreased in a dose-dependent manner. The cell survival curve showed SF2, α, and β values to be 0.568, 0.209, and 0.020 respectively. At 200y irradiated cells showed higher optical density than the control group. After irradiation, apoptosis was not observed but G2 arrest was observed in the NHOK cells. 1 day after 10 Gy irradiation, the expression of p53 remained unchanged, the p2l/sup WAF1/Cipl/ increased and the mdm2 decreased. The expression of bax, bcl-2, cyclin B1, and cyclin D remained unchanged. Conclusion: These results indicate that NHOK responds to irradiation by G2 arrest, which is possibly mediated by the expression of p21/sup WAFl/Cipl/, and that cell necrosis occurs by high dose irradiation.

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임프란트에 관련된 금속이온의 조골세포에 대한 세포독성에 미치는 Hsp27의 영향에 대한 실험적 연구 (HSP27 MODULATION OF IMPLANT- ASSOCIATED METAL ION CYTOTOXICITY OF OSTEOBLASTIC CELLS)

  • 윤정호;하동진;임재석;권종진;장현석;이의석;김대성
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제28권2호
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    • pp.127-135
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    • 2006
  • Objectives: The extent of bone formation that occurs at the interface of metallic implants and bone is determined by the number and activity of osteoblastic cells. Stress proteins may be contributing determinants of cell viability in altered environments. Hsp27 is a small Mr hsp which is known as a molecular chaperone. Methods: To better understand how heat shock protein 27 contributes to endosseous implant - associated metal ions affects on osteoblastic cell viability, the effect of chromium and titanium ions were compared to effects of cadmium ions in the ROS17/2.8 osteoblastic cell line. Results: ROS17/2.8 osteoblastic cell line demonstrated ion - specific reductions in growth; reductions were significantly greater for cadmium than for chromium or titanium. Chromium impaired growth of cultures without altering cell viability measured using the MTT assay. A stable transformed cell line expressing additional hsp27(clone "A7") was resistant to the toxic effects of titanium and partially protected from cadmium toxicity. Conclusions: A role for hsp27 in protection of osteoblastic cells from metal ion toxicity is supported by the chromium - induced elevations in hsp27 abundance and the behavior of the A7 cell line in response to metal ions in culture. Similar biochemical responses to altered cellular environments may contribute to the fate of tissues adjacent to select metallic implants.

상아질성 유령세포종양: 증례보고와 문헌고찰 (Dentinogenic Ghost Cell Tumor: A Case Report and Review of Literature)

  • 김성민;최소영;이재일;허경회;명훈;이종호
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제35권1호
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    • pp.66-71
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    • 2013
  • Dentinogenic ghost cell tumor (DGCT) is a rare epithelial odontogenic neoplasm, representing 1.9% to 2.1% of all odontogenic tumors. It is the neoplastic counterpart of the calcifying odontogenic cyst (COC), and characteristic islands of odontogenic epithelical cells contain numerous ghost cells and dysplastic dentin, and also have many common histological features with ameloblastoma. The 2005 World Health Organization (WHO) Classification of Odontogenic Tumours re-named this entity as calcifying cystic odontogenic tumor (CCOT) and defined the clinico-pathological features of the ghost cell odontogenic tumours, CCOT, DGCT and ghost cell odontogenic carcinoma (GCOC). We report a rare case of central DGCT in the posterior maxilla of a 31-year-old female with literature review, for the emphasis of Oral and Maxillofacial surgeon's role.

Bradykinin-induced $Ca^{2+}$ signaling in human oral squamous cell carcinoma HSC-3 cells

  • Sohn, Byung-Jin;Kang, Ji-Ah;Jo, Su-Hyun;Choi, Se-Young
    • International Journal of Oral Biology
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    • 제34권2호
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    • pp.73-79
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    • 2009
  • Cytosolic $Ca^{2+}$ is an important regulator of tumor cell proliferation and metastasis. Recently, the strategy of blocking receptors and channels specific to certain cancer cell types has emerged as a potentially viable future treatment. Oral squamous cell carcinoma is an aggressive form of cancer with a high metastasis rate but the receptor-mechanisms involved in $Ca^{2+}$ signaling in these tumors have not yet been elucidated. In our present study, we report that bradykinin induces $Ca^{2+}$ signaling and its modulation in the human oral squamous carcinoma cell line, HSC-3. Bradykinin was found to increase the cytosolic $Ca^{2+}$ levels in a concentration-dependent manner. This increase was inhibited by pretreatment with the phospholipase C-${\beta}$ inhibitor, U73122, and also by 2-aminoethoxydiphenyl borate, an inhibitor of the inositol 1,4,5-trisphosphate receptor. Pretreatment with extracellular ATP also inhibited the peak bradykinin-induced $Ca^{2+}$ rise. In contrast, the ATP-induced rise in cytosolic $Ca^{2+}$ was not affected by pretreatment with bradykinin. Pretreatment of the cells with either forskolin or phorbol 12-myristate 13-acetate (activators of adenylyl cyclase and protein kinase C, respectively) prior to bradykinin application accelerated the recovery of cytosolic $Ca^{2+}$ to baseline levels. These data suggest that bradykinin receptors are functional in $Ca^{2+}$ signaling in HSC-3 cells and may therefore represent a future target in treatment strategies for human oral squamous cell carcinoma.

Transglutaminase 2 mRNA Expression in Salivary Gland Tumor Cell Line

  • Chun, Yoon Kwon;Lee, Chong Heon
    • Journal of Korean Dental Science
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    • 제6권1호
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    • pp.22-26
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    • 2013
  • Purpose: Transglutaminase 2 (TGase 2) is expressed by tumor necrosis factor-${\alpha}$ in various carcinoma. The role of TGase 2 expression in salivary gland tumors is not clear yet. Established slaivary gland tumor (SGT)cell line has been used to study the pathogenesis of salivary gland adenocarcinoma on a cellular level in vitro. The pupose of this study were to examine mRNA expression of TGase 2 in SGT cell line compared to other tumor cell lines, and to apply these results to the pathogenesis of salivary gland tumor. Materials and Methods: After SGT, SCC-15, HN 4, and HeLa tumor cell lines were cultured under preconfl uency, and 3 days after postconfl uency, the cells were harvested for total RNA extraction and cDNA preparation. Result: Reverse transcription polymerase chain reaction for semiquantitative mRNA analysis was done. TGase 2 mRNA expression was not induced by confl uency in all the cell lines. TGase 2 mRNA expression was variable but markedly enhanced in SGT cell line. Conclusion: mRNA expression of TGase 2 should play an important role in the pathogenesis of SGT cell line originated from ductal cell.

Ankyrin Repeat-Rich Membrane Spanning (ARMS)/Kidins220 Scaffold Protein Regulates Neuroblastoma Cell Proliferation through p21

  • Jung, Heekyung;Shin, Joo-Hyun;Park, Young-Seok;Chang, Mi-Sook
    • Molecules and Cells
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    • 제37권12호
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    • pp.881-887
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    • 2014
  • Cell proliferation is tightly controlled by the cell-cycle regulatory proteins, primarily by cyclins and cyclin-dependent kinases (CDKs) in the $G_1$ phase. The ankyrin repeat-rich membrane spanning (ARMS) scaffold protein, also known as kinase D-interacting substrate of 220 kDa (Kidins 220), has been previously identified as a prominent downstream target of neurotrophin and ephrin receptors. Many studies have reported that ARMS/Kidins220 acts as a major signaling platform in organizing the signaling complex to regulate various cellular responses in the nervous and vascular systems. However, the role of ARMS/Kidins220 in cell proliferation and cell-cycle progression has never been investigated. Here we report that knockdown of ARMS/Kidins220 inhibits mouse neuroblastoma cell proliferation by inducing slowdown of cell cycle in the $G_1$ phase. This effect is mediated by the upregulation of a CDK inhibitor p21, which causes the decrease in cyclin D1 and CDK4 protein levels and subsequent reduction of pRb hyperphosphorylation. Our results suggest a new role of ARMS/Kidins220 as a signaling platform to regulate tumor cell proliferation in response to the extracellular stimuli.

수종의 암세포주의 저선량 방사선감수성에 관한 실험적 연구 (AN EXPERIMENTAL STUDY ON THE LOW-DOSE RADIOSENSITIVITY OF TUMOR CELL LINES)

  • 김민숙;고광준
    • 치과방사선
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    • 제24권2호
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    • pp.249-260
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    • 1994
  • The purpose of this study was to aid in the radiation therapy of head and neck cancer patients. For this study, radiation survival curves were generated for Bl6, MG-63 and YAC-l cell lines using semiautomated MTT assay and Dye Exclusion Assay. Irradiation of 2, 4, 6, 8, 10Gy were delivered at room temperature at a dose rate of 210.2cGy/min using / sup 60/Co γ-ray Irradiator ALOORAOO 8. The viable cells were determined for each radiation dose and compared to control values. The obtained results were as follows: 1. There was significantly different absorbance at 10Gy on B16 cell line in MTT assay(P<0.05). 2. There was significantly different absorbance at 4, 6, 8, 10Gy on MG-63 cell line in MTT assay(P<0.05). 3. YAC-l cell line was more sensitive than B16 or MG-63 cell line to all doses of radiation(P<0.05). 4. There was significantly different absorbance among all tumor cell lines except between B16 and MG-63 cell line at ZGy in MTT assay(P<0.05). 5. Good correlation was obtained between MTT assay and DEA(P<0.05). The efficient of correlation of B16, MG-63 and YAC-l cell line was 0.845, 0.824 and 0.906, respectively.

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치성낭종으로부터 유래된 편평상피세포암종 (SQUAMOUS CELL CARCINOMA ARISING FROM RESIDUAL ODONTOGENIC CYST;Report of a Case & Review of Literatures)

  • 김용각;박형국;권혁진;현재훈
    • Maxillofacial Plastic and Reconstructive Surgery
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    • 제19권2호
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    • pp.209-214
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    • 1997
  • Odontogenic cysts are relatively common pathologic lesions found in the oral and perioral structures, but the case of squamous cell carcinoma arising from those cysts are very uncommon. After first reported of that case in 1889 by Herman, Schwimmer collected 56 cases of previously reported squamous cell carcinoma arising in residual odontogenic cyst during about past one century. More than 60% of cases of carcinoma developing in odontogenic cysts arising in inflammatory periapical or residual cyst, and these tumors are usually well-differentiated with relatively good prognosis, and often are diagnosed as benign lesion in radiographic or clinical examination, therefore definitive diagnosis must be made by histologic examintation. We report a case and review the literatures, in our case, 78-year old woman were clinically and radiographically diagnosed as residual odontogenic cyst. But in histologic examination after enucleation of lesion, mass of squamous cell carinoma were observed, but in other area, typical cyst wall and lining epithelium were observed. And in some area, carcinoma in situ and invading squamous cell carcinoma into the lining epithelium were also observed.

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Radiation-induced Apoptosis, Necrosis and G2 Arrest in Fadu and Hep2 Cells

  • Lee Sam-Sun;Kang Beom-Hyun;Choi Hang-Moon;Jeon In-Seong;Heo Min-Suk;Choi Soon-Chul
    • Imaging Science in Dentistry
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    • 제30권4호
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    • pp.275-279
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    • 2000
  • Purpose: Radiation damage is produced and viable cell number is reduced. We need to know the type of cell death by the ionizing radiation and the amount and duration of cell cycle arrest. In this study, we want to identified the main cause of the cellular damage in the oral cancer cells and normal keratinocytes with clinically useful radiation dosage. Materials and Methods: Human gingival tissue specimens obtained from healthy volunteers were used for primary culture of the normal human oral keratinocytes (NHOK). Primary NHOK were prepared from separated epithelial tissue and maintained in keratinocyte growth medium containing 0.15 mM calcium and a supplementary growth factor bullet kit. Fadu and Hep-2 cell lines were obtained from KCLB. Cells were irradiated in a /sup 137/Cs γ-irradiator at the dose of 10 Gy. The dose rate was 5.38 Gy/min. The necrotic cell death was examined with Lactate Dehydrogenase (LDH) activity in the culture medium. Every 4 day after irradiation, LDH activities were read and compared control group. Cell cycle phase distribution and preG1-incidence after radiation were analyzed by flow cytometry using Propidium Iodine staining. Cell cycle analysis were carried out with a FAC Star plus flowcytometry (FACS, Becton Dickinson, USA) and DNA histograms were processed with CELLFIT software (Becton Dickinson, USA). Results: LDH activity increased in all of the experimental cells by the times. This pattern could be seen in the non-irradiated cells, and there was no difference between the non-irradiated cells and irradiated cells. We detected an induction of apoptosis after irradiation with a single dose of 10 Gy. The maximal rate of apoptosis ranged from 4.0% to 8.0% 4 days after irradiation. In all experimental cells, we detected G2/M arrest after irradiation with a single dose of 10 Gy. Yet there were differences in the number of G2/M arrested cells. The maximal rate of the G2/M ranges from 60.0% to 80.0% 24h after irradiation. There is no significant changes on the rate of the G0/G1 phase. Conclusion: Radiation sensitivity was not related with necrosis but cell cycle arrest and apoptosis. These data suggested that more arrested cell is correlated with more apoptosis.

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구강암의 조직비반세포에 관한 연구

  • 전동진
    • 대한치과의사협회지
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    • 제12권1호
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    • pp.21-28
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    • 1974
  • The author has observed the distribution of the tissue mast cells in 67 various tumors and precancerous lesions which occurred in the oral cavity. The specimcns ware obtained from the department of oral pathology, college of dentistry, Seoul National University, from Jan. 1970 to June, 1973. The results are as follows: 1) The number of the tissue mast cell was decrease predominantly in malignant tumors, especially in squamous cell carcinomas and in sarcomas. 2) The number of the tissue mast cell distirbution in adenocarcinomas one of malignant group was sligtly increased in with healthy oral mucosa. 3) The number of tissue mast cells in ameloblastomas one of benign group of the tumor of epithelial originwas more decreased than that in healthy oral mucosa. 4) The number of tissue mast cells in fibromas was more than that in healthy oral mucosa. 5) The number of the tissue mast cells in mixed tumors was increased one and a half times as many as that in healthy oral mucosa. 6) The number of the tissue mast cells in mixed tumors was increased one and a half times as many as that in healthy oral mucosa. 7) The tissue mast cell distribution can be observed more densly in the stroma of tumors than in the parenchyme of tumors.

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