• 제목/요약/키워드: Adhesion Promoter

검색결과 49건 처리시간 0.024초

WAVEs: A Novel and Promising Weapon in the Cancer Therapy Tool Box

  • Sakthivel, K.M.;Prabhu, V. Vinod;Guruvayoorappan, C.
    • Asian Pacific Journal of Cancer Prevention
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    • 제13권5호
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    • pp.1719-1722
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    • 2012
  • The Wiskott-Aldrich Syndrome Protein family Verprolin - homologous proteins (WAVEs), encoded by a metastasis promoter gene, play considerable roles in adhesion of immune cells, cell proliferation, migration and destruction of foreign agents by reactive oxygen species. These diverse functions have lead to the hypothesis that WAVE proteins have multi-functional roles in regulating cancer invasiveness, metastasis, development of tumor vasculature and angiogenesis. Differentials in expression of WAVE proteins are associated with a number of neoplasms include colorectal cancer, hepatocellular cancer, lung squamous cell carcinoma, human breast adenocarcinoma and prostate cancer. In this review we attempt to unify our knowledge regarding WAVE proteins, focusing on their potentials as diagnostic markers and molecular targets for cancer therapy.

The 14-3-3 Gene Function of Cryptococcus neoformans Is Required for its Growth and Virulence

  • Li, Jingbo;Chang, Yun C.;Wu, Chun-Hua;Liu, Jennifer;Kwon-Chung, Kyung J.;Huang, Sheng-He;Shimada, Hiro;Fante, Rob;Fu, Xiaowei;Jong, Ambrose
    • Journal of Microbiology and Biotechnology
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    • 제26권5호
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    • pp.918-927
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    • 2016
  • Cryptococcus neoformans is a life-threatening pathogenic yeast that causes devastating meningoencephalitis. The mechanism of cryptococcal brain invasion is largely unknown, and recent studies suggest that its extracellular microvesicles may be involved in the invasion process. The 14-3-3 protein is abundant in the extracellular microvesicles of C. neoformans, and the 14-3-3-GFP fusion has been used as the microvesicle's marker. However, the physiological role of 14-3-3 has not been explored. In this report, we have found that C. neoformans contains a single 14-3-3 gene that apparently is an essential gene. To explore the functions of 14-3-3, we substituted the promoter region of the 14-3-3 with the copper-controllable promoter CTR4. The CTR4 regulatory strain showed an enlarged cell size, drastic changes in morphology, and a decrease in the thickness of the capsule under copper-enriched conditions. Furthermore, the mutant cells produced a lower amount of total proteins in their extracellular microvesicles and reduced adhesion to human brain microvascular endothelial cells in vitro. Proteomic analyses of the protein components under 14-3-3-overexpressed and -suppressed conditions revealed that the 14-3-3 function(s) might be associated with the microvesicle biogenesis. Our results support that 14-3-3 has diverse pertinent roles in both physiology and pathogenesis in C. neoformans. Its gene functions are closely relevant to the pathogenesis of this fungus.

Sodium butyrate에 의한 E-cadherin의 발현증가와 세포간 상호작용의 변화 (Sodium Butyrate Alters Cell-Cell Interactions through Up-Regulation of E-Cadherin in Human Hepatocellular Carcinoma Cells)

  • 권현진;장경립
    • 생명과학회지
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    • 제19권6호
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    • pp.705-710
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    • 2009
  • Sodium butyrate (NaBt)는 장에서 탄수화물대사로부터 생겨나는 짧은 천연지방산 사슬로 다양한 인간 암세포들 에게서 강력한 항암효능을 나타냄이 보고된 바 있지만 자세한 기전은 아직 알려져 있지 않다. 이 논문에서 우리는 NaBt가 주요 세포부착분자이면서 종양억제인자의 일종인 E-cadherin의 발현을 세포-특이적으로 촉진하는 기전을 연구하였다. 또한 NaBt는 E-eadherin의 발현을 촉진하는 것으로 알려진 p21의 발현도 증가시켰지만, NaBt에 의하여 증가한 p21은 E-cadherin의 활성화와 관련이 없음이 밝혀졌다. 그 대신에 NaBt는 CCAAT-box를 통한 E-cadherin 유전자의 프로모터 활성을 증가시킴으로써 E-cadherin의 발현을 전사수준에서 촉진하는 것 같다. 이렇게 NaBt에 의하여 증가된 E-cadherin은 주로 세포간 접촉면에 위치하면서 Hep3B 세포를 더 분화된 형태로 유도하여 NaBt의 항암활성이 나타나는 것 같다.

Lactosylceramide Mediates the Expression of Adhesion Molecules in TNF-${\alpha}$ and IFN ${\gamma}$-stimulated Primary Cultured Astrocytes

  • Lee, Jin-Koo;Kim, Jin-Kyu;Park, Soo-Hyun;Sim, Yun-Beom;Jung, Jun-Sub;Suh, Hong-Won
    • The Korean Journal of Physiology and Pharmacology
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    • 제15권5호
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    • pp.251-258
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    • 2011
  • Here we have investigated how lactosylceramide (LacCer) modulates gene expression of adhesion molecules in TNF-${\alpha}$ and IFN ${\gamma}$ (CM)-stimulated astrocytes. We have observed that stimulation of astrocytes with CM increased the gene expression of ICAM-1 and VCAM-1. D-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and N-butyldeoxynojirimycin (NBDNJ), inhibitors of glucosylceramide synthase (GLS) and LacCer synthase (galactosyltransferase, GalT-2), inhibited the gene expression of ICAM-1 and VCAM-1 and activation of their gene promoter induced by CM, which were reversed by exogenously supplied LacCer. Silencing of GalT-2 gene using its antisense oligonucleotides also attenuated CM-induced ICAM-1 and VCAM-1 expression, which were reversed by LacCer. PDMP treatment and silencing of GalT-2 gene significantly reduced CM-induced luciferase activities in NF-${\kappa}B$, AP-1, GAS, and STAT-3 luciferase vectors-transfected cells. In addition, LacCer reversed the inhibition of NF-${\kappa}B$ and STAT-1 luciferase activities by PDMP. Taken together, our results suggest that LacCer may play a crucial role in the expression of ICAM-1 and VCAM-1 via modulating transcription factors, such as NF-${\kappa}B$, AP-1, STAT-1, and STAT-3 in CM-stimulated astrocytes.

Loss of Expression and Aberrant Methylation of the CDH1 (E-cadherin) Gene in Breast Cancer Patients from Kashmir

  • Asiaf, Asia;Ahmad, Shiekh Tanveer;Aziz, Sheikh Aejaz;Malik, Ajaz Ahmad;Rasool, Zubaida;Masood, Akbar;Zargar, Mohammad Afzal
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권15호
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    • pp.6397-6403
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    • 2014
  • Background: Aberrant promoter hypermethylation has been recognized in human breast carcinogenesis as a frequent molecular alteration associated with the loss of expression of a number of key regulatory genes and may serve as a biomarker. The E-cadherin gene (CDH1), mapping at chromosome 16q22, is an intercellular adhesion molecule in epithelial cells, which plays an important role in establishing and maintaining intercellular connections. The aim of our study was to assess the methylation pattern of CDH1 and to correlate it with the expression of E-cadherin, clinicopathological parameters and hormone receptor status in breast cancer patients of Kashmir. Materials and Methods: Methylation specific PCR (MSP) was used to determine the methylation status of CDH1 in 128 invasive ductal carcinomas (IDCs) paired with the corresponding normal tissue samples. Immunohistochemistry was used to study the expression of E-cadherin, ER and PR. Results: CDH1 hypermethylation was detected in 57.8% of cases and 14.8% of normal adjacent controls. Reduced levels of E-cadherin protein were observed in 71.9% of our samples. Loss of E-cadherin expression was significantly associated with the CDH1 promoter region methylation (p<0.05, OR=3.48, CI: 1.55-7.79). Hypermethylation of CDH1 was significantly associated with age at diagnosis (p=0.030), tumor size (p=0.008), tumor grade (p=0.024) and rate of node positivity or metastasis (p=0.043). Conclusions: Our preliminary findings suggest that abnormal CDH1 methylation occurs in high frequencies in infiltrating breast cancers associated with a decrease in E-cadherin expression. We found significant differences in tumor-related CDH1 gene methylation patterns relevant to tumor grade, tumor size, nodal involvement and age at diagnosis of breast tumors, which could be extended in future to provide diagnostic and prognostic information.

조각자(皂角刺)가 악성흑색종 세포주에 미치는 영향 (Pathways Analysis of Gleditsia spina Extract on Changes of Gene Expression in Human Melanoma cells)

  • 김부여;임세현;이병호;임지연;김용성;조수인
    • 한방안이비인후피부과학회지
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    • 제22권3호
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    • pp.47-62
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    • 2009
  • Glenditsia spina (GS) can resolve carbuncle, relive swelling, dispel wind and destroy parasites. For these reasons, GS has been widely used as dermatologic agent clinically. In this study, the specific pathways of anti-proliferative effect of GS on human derived melanoma cells were identified. The molecular profile was measured using microarray technique to identify up- or down-regulated genes in SK-MEL-2 cell line. Pathway analysis was done by listing percentage of pathway involvement, and the represented pathways were obtained from KEGG. The transcription factor binding sequences were obtained by Transfac database. By the promoter analysis, up-regulated genes by GS were mainly associated with MAPK, Regulation of actin cytoskeleton, Wnt, Focal adhesion and Long term potentiation pathway. Down-regulated genes by GS were mainly associated with MAPK and Antigen processing and presentation pathway. And some of the transcription factors like Sp1 and NF-Y in up-regulated genes and Oct-1 in down-regulated genes by GS also identified.

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Cu 배선에 Al층간 물질 첨가에 의한 EM특성 개선 (Improvement of electromigration characteristics in using Ai interlayer)

  • 이정환;박병남;최시영
    • 한국진공학회지
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    • 제10권4호
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    • pp.403-410
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    • 2001
  • 본 연구에서는 차세대 Cu 박막 증착 방법으로 유망한 CVD(chemical vapor deposition)방법으로 실질적 배선 증착 공정과 동일하게 시행하여 여러 조건에서 Cu를 증착하여 가장 EM에 관하여 높은 내구성을 가지는 조건을 알아보고 또한 박막의 미세구조가 EM에 어떠한 영향을 미치는지를 알아보았으며 MOCVD 방식으로 증착한 Cu박막의 표면과 barrier layer인 TiN과의 응력(stress)을 조사하여 차세대 EM모델인 grain boundary grooving 모델에 실질적으로 적용하였다. 또한, 이러한 실험을 행 한 후에 정확한 EM 현상을 관찰하고 분석하여 반도체 소자의 신뢰성과 성능개선, 결함 예측, 그리고 소자의 배선설계에 중요한 정보를 제공할 것이다. 또한, 보다 우수한 EM 특성을 가질 수 있게 하기 위해 barrier layer위에 Cu와의 접착력(adhesion)을 향상시킬 수 있는 promoter로 Al을 이용하여 얇게 증착한 후 EM축적 파괴 실험을 하여 EM에 대한 높은 저항성을 실질적으로 가질 수 있는지에 대한 실험도 병행하였다.

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저온소성 프릿이 첨가된 MnWO4의 소결체의 습도특성 (Humidity Properties of Sintered MnWO4 with a Low Temperature Firing Frit)

  • 정병해;소지영;김형순
    • 한국재료학회지
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    • 제13권2호
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    • pp.120-125
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    • 2003
  • A low melting borosilicate glass frit was used as an adhesion promoter, which enables $MnWO_4$to be sintered with in a reasonable sintering temperature range ($800∼1000^{\circ}C$). The glass was evaluated for glass transition temperature ($Τ_{g}$ X) and thermal expansion coefficient($\alpha$). Mechanical property (Vickers hardness), grain growth, the comparison of lattice parameter and pore distribution of sintered $MnWO_4$ with the frit were methodically discussed. As sintering temperature increased, a typical liquid phase sintering showed the rapid grain growth and high densification of X$MnWO_4$grain, improvement of hardness (until $920^{\circ}C$) and different pore size distribution. Resistance of sintered $MnWO_4$varied from 450k$\Omega$ to 8.8M$\Omega$ under the measuring humidify ranging from 30 to 90%. Thus, the results will contribute to the application of glass frit containing sensor materials and their future use.

법랑아세포종에서 p16과 E-cadherin의 메틸화 (Methylation of p16 and E-cadherin in ameloblastoma)

  • 박찬웅;윤혜경;박상준
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • 제36권6호
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    • pp.453-459
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    • 2010
  • Introduction: Ameloblastic carcinoma is a rare malignant lesion, and may arise from either carcinoma ex-ameloblastoma or de novo carcinoma. Aberrant promoter hypermethylation of the tumor-associated genes leading to their inactivation is a common event in many cancer types. The p16/CDKN2/INK4A gene and p16 5 protein are involved directly in regulating the cell cycles. Cadherins are cell adhesion molecules that modulate the epithelial phenotype and regulate tumor invasion. The aim of this study was to evaluate the roles of p16 and E-cadherin methylation and loss of p16 and E-cadherin expression in the malignant transformation of an ameloblastoma. Materials and Methods: Eight cases of ameloblastoma, including 4 benign ameloblastomas without recurrence, 2 benign ameloblastomas with recurrence and 2 carcinoma ex-ameloblastomas, were examined. The promoter hypermethylation profile of the p16 and E-cadherin genes was studied using methylation-specific polymerase chain reaction (MSP) and immunohistochemical staining for p16 and E-cadherin expression. Results: 1) Aberrant CpG island methylation of the p16 gene was detected in 3 of the 4 benign ameloblastomas without recurrence and 1 of the 2 benign ameloblastomas with recurrence. 2) Aberrant CpG island methylation of the E-cadherin gene was found in 1 of the 4 benign ameloblastomas without recurrence. 3) A loss of p16 expression was noted in 1 of 4 benign ameloblastomas without recurrence and 1 of 2 carcinoma ex-ameloblastomas. 4) A loss of E-cadherin expression was noted in 2 of the 4 benign ameloblastomas without recurrence, 1 of the 2 benign ameloblastomas with recurrence and 2 of the 2 carcinoma ex-ameloblastomas. 5) A loss of p16 expression was observed in 1 of the 4 cases showing aberrant methylation of the p16 gene. 6) A loss of E-cadherin expression was observed in 3 benign ameloblastoma case showing aberrant methylation of the E-cadherin gene. Conclusion: These results suggest that loss of E-cadherin expression related to the other genetic pathway (not methylation) might be an adjuvant indicator predicting the malignant transformation of an ameloblastoma. However, the number of samples in this study was too small and the relationship between the treatment methods and clinical course were not defined. Therefore, further study will be needed.