1.A Potent Metastatic Factor in Squamous Cell Carcinoma: Laminin 332.
Soon Young KWON ; William B CARPENTER ; Philip M CARPENTER
Korean Journal of Otolaryngology - Head and Neck Surgery 2008;51(11):956-959
No abstract available.
Cell Adhesion Molecules
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Laminin
2.The Role of Cell Adhesion Molecules in the Modulation of Chondrocytes-extracellular Type II Collagen by Transforming Growth Factor-beta1.
Jin Woo LEE ; Eung Chick KANG ; Soo Bong HAHN ; Sung Jae KIM ; Yun Hee KIM ; Su Hyang KIM ; Sean P SCULLY
Journal of Korean Orthopaedic Research Society 2001;4(1):32-42
No Abstract Available.
Cell Adhesion Molecules*
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Cell Adhesion*
;
Collagen Type II*
3.Integrin activation, focal adhesion maturation and tumor metastasis.
Meng-Wen HUANG ; Chang-Dong LIN ; Jian-Feng CHEN
Acta Physiologica Sinica 2021;73(2):151-159
Integrins are a large family of heterodimeric cell adhesion molecules composed of α and β subunits. Through interaction with their specific ligands, integrins mediate cell-cell and cell-extracellular matrix interactions. Via outside-in signaling, integrins can recruit cytoplasmic proteins to their intracellular domains and then cluster into supramolecular structures and trigger downstream signaling. Integrin activation is associated with a global conformation rearrangement from bent to extended in ectodomains and the separation of α and β subunit cytoplasmic domains. During cell migration, integrins regulate the focal adhesion dynamics and transmit forces between the extracellular matrix and the cell cytoskeleton. In tumor microenvironment, integrins on multiple kinds of cells could be activated, which modulates cell migration into tumor and contributes to angiogenesis and tumor metastasis. Here, we review the mechanism of integrin activation, dynamics of focal adhesions during cell migration and tumor metastasis.
Cell Adhesion
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Cell Adhesion Molecules
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Focal Adhesions
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Integrins
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Signal Transduction
4.The Effect of low-dose Aspirin and Clomiphene Citrate on the Expression of Neural Cell Adhesion Molecules (NCAM) in the Human Endometrium.
Jung Han LEE ; Jung Hye HWANG ; Seung Ryong KIM ; Young Jin MOON ; Moon Il PARK ; Sung Ro CHUNG ; Hyung MOON ; Youn Yeung HWANG ; Se Jin JANG ; Il Kyu PARK
Korean Journal of Obstetrics and Gynecology 2001;44(9):1596-1601
OBJECTIVE: The treatment with low-dose aspirin in the patients with unexplained infertility has been reported to improve the pregnancy rate and implantation rate via increasing the blood flow in the endometrium. But there are little known about the relationships between low-dose aspirin and cell adhesion molecules, NCAM. The aim of this study was to evaluate the effect of low-dose aspirin and clomiphene citrate treatment on the expression of NCAM in the endometrium. METHODS: The patients with unexplained infertility (N=37) were grouped into 3 groups: clomiphene citrate and low-dose aspirin treated group (N=8), clomiphene citrate treated group (N=10), and natural cycle group (N=10, no treatment). As control group, the proliferative and menopausal endometrium was used. Each endometium was obtained by endometrial biopsy performed in late luteal phase and immunohistochemical staining with NCAM was performed. RESULTS: In the stromal cells, the staining intensity of NCAM expression and the number of vessels were significantly increased in the endomterium treated with clomiphene citrate and low-dose aspirin compared with other groups (p<0.05). And the expression of NCAM in the prolifertive and menopausal endometrium showed very weak staining. CONCLUSION: The expression of NCAM in the stromal cells and the number of vessels were increased in the endometrium of unexplained infertility patients treated with clomiphene citrate and low-dose aspirin. These findings may suggest low-dose aspirin has an important role during the secretory phase of endometrium to improve the implantation via increasing the expression of cell adhesion molecules, especially NCAM and increasing the number of vessels.
Aspirin*
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Biopsy
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Cell Adhesion Molecules
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Clomiphene*
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Endometrium*
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Female
;
Humans*
;
Infertility
;
Luteal Phase
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Neural Cell Adhesion Molecules*
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Pregnancy Rate
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Stromal Cells
5.The expression of NCAM ( Neural Cell Adhesion Molecule) in myometrium and leiomyoma.
Eun Hee YOO ; Eun Mi WHANG ; Hye Sung MOON ; Hae Soo KOO ; Jong Il KIM ; Han Ki YU
Korean Journal of Obstetrics and Gynecology 2000;43(10):1808-1812
No abstract available.
Animals
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Cell Adhesion*
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Female
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Leiomyoma*
;
Mice
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Myometrium*
;
Neural Cell Adhesion Molecules*
6.Cell adhesion and synaptogenesis.
Gong CHEN ; Xia WU ; Sebnem TUNCDEMIR
Acta Physiologica Sinica 2007;59(6):697-706
Synapses are inter-neuronal connections that are fundamental working units in neural networks. How synapses are molecularly constructed is a fascinating question, which attracted scientists' attention for many decades. Neuromuscular junction, a field pioneered by Te-Pei FENG and many others, has been an excellent model for studying synaptogenesis and paved the way for our understanding of the synapse formation in the central nervous system. Recent studies shed new light on the molecular mechanisms of central synapse formation by discovering a group of cell adhesion molecules exerting potent synaptogenic effects. This review will focus on those cell adhesion molecules which can induce central synapse formation when expressed in non-neuronal cells.
Cell Adhesion
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Cell Adhesion Molecules
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physiology
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Humans
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Neuromuscular Junction
;
physiology
;
Synapses
;
physiology
7.Progress on the role of synaptic cell adhesion molecules in stress.
Acta Physiologica Sinica 2020;72(2):220-226
Synaptic cell adhesion molecules (CAMs) are a type of membrane surface glycoproteins that mediate the structural and functional interactions between pre- and post-synaptic sites. Synaptic CAMs dynamically regulate synaptic activity and plasticity, and their expression and function are modulated by environmental factors. Synaptic CAMs are also important effector molecules of stress response, and mediate the adverse impact of stress on cognition and emotion. In this review, we will summarize the recent progress on the role of synaptic CAMs in stress, and aim to provide insight into the molecular mechanisms and drug development of stress-related disorders.
Cell Adhesion
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Cell Adhesion Molecules
;
physiology
;
Humans
;
Neuronal Plasticity
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Stress, Physiological
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Stress, Psychological
;
Synapses
8.Progress of epithelial-mesenchymal transition in respiratory system and the modulatory mechanism of cell adhesion.
Mei-Ling TAN ; Chun-Jiao LONG ; Wang JIANG ; Jin-Mei WANG ; Jiao PI ; Xiao-Qun QIN ; Yang XIANG
Acta Physiologica Sinica 2020;72(5):605-616
Epithelial-mesenchymal transition (EMT) plays an important role in the development and pathogenesis of respiratory system. Epithelial cells are characterized by well-developed, intercellular contacts, whereas EMT triggers the sequential destabilization of cell-cell adhesive junctions. The dynamic remodeling of the epithelial cell adhesion molecules is important for maintaining the integrity and normal function of epithelium. This paper reviews the research progress of EMT in lung development, lung injury repair and chronic lung diseases, and summarizes the effect of cell junctions and cell adhesion molecules on EMT molecular events.
Cell Adhesion
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Cell Adhesion Molecules
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Epithelial Cells
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Epithelial-Mesenchymal Transition
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Respiratory System
9.Effect of Quercetin on the Cell Cycle and Adhesion Molecules of NOD/SCID Mice with Acute B Lymphocytic Leukemia.
Li WANG ; Hong-Wei DAI ; Jun ZHENG ; Jiao ZHOU ; De-Sen CHEN
Journal of Experimental Hematology 2018;26(6):1616-1620
OBJECTIVE:
To investigate the effect of Quercetin on cell cycle and adhesive molecules of NOD.SCID mice with acule B lymphocytic leuaemia(B-ALL).
METHODS:
5×10 Nalm-6(B-ALL cell line) cells were injected into the tail vein of 48 NOD/SCID mice to establish the NOD/SCID mice with B-ALL. After 15 day, the NOD/SCID mice with B-ALL were randomly divided into 3 groups: salive group as control (injection with saline of 0.2 ml/mouse), cyclophos-phamid group (injection with cyclophosphamide of 100µg/kg) and quercetin group(injection with quercetin of 3 mg/kg). After treatment for 21 d, the perecntage of Nalm-6 cells in G1, G2, M and S phases was detected by flow cytonetry; the B lymphocytes Nalm-6 cells, neutrophils and WBC in while blood were counted before and after treatment; the expression of intercellalar. Adhesion molecole-1(FCAIU-1), vascular cell adhesion molecule-1(VCAM-1) and P-selectin was detected by double autibody soundwich method.
RESULTS:
Compared with level before treatment, the expression of ICAM-1, VCAM-1 and P-selectin decreased after treatment with guercetin, The hemogram showed that the peripheral blood nentrophil level obviously increased, while the levels of B lymphocytes, Nalm-6 cells and WBC count decreased obviously after treatment with guercetin. The cell proliferatim rario in G0/G1 phase decreased, yet the cell proliferation ratio in S and G2/M phases increased after treatment with guercetin.
CONCLUSION
The guercetin can decrease the intercellular adhesion through inhibition of ICAM-1 expression, and arrests Nalm-6 cells in S and G2/M phases. The guercetin has obviously inhibitory effect on B-ALL cells.
Animals
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Cell Adhesion
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Cell Adhesion Molecules
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Intercellular Adhesion Molecule-1
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Leukemia, B-Cell
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Mice
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Mice, Inbred NOD
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Mice, SCID
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Quercetin
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Vascular Cell Adhesion Molecule-1
10.Luteolin reverses OPCML methylation to inhibit proliferation of breast cancer MDA-MB-231 cells.
Xinmin DONG ; Ti ZHENG ; Ziying ZHANG ; Xiling BAI ; Hua LI ; Jian ZHANG
Journal of Southern Medical University 2020;40(4):550-555
OBJECTIVE:
To observe the effect of luteolin on the proliferation and expression of OPCML in breast cancer cell line MDA-MB-231.
METHODS:
Cultured MDA-MB-231 cells were treated with luteolin at the concentrations of 5, 10 and 20 μmol/L for 24 or 48 h. MTT assay was used to detect cell proliferation and flow cytometry was used to detect the cell apoptosis. The expressions of OPCML mRNA and protein were detected using real-time quantitative PCR and Western blotting, respectively. OPCML gene methylation in the promoter region was detected using methylation-specific PCR (MSP), and the activity of methylase in the cells was analyzed.
RESULTS:
MTT assay showed that treatment with luteolin at 5, 10 and 20 μmol/L for 24 h concentration-dependently decreased the viability of MDA-MB-231 cells ( < 0.05). Flow cytometry also showed that luteolin at different concentrations could induce apoptosis of MDA-MB-231 cells ( < 0.05). Luteolin dose-dependently induced the expression of OPCML mRNA and protein in MDA-MB-231 cells ( < 0.05), down-regulated the methylation status in the promoter region of OPCML gene, up-regulated the level of non-methylated OPCML, and reduced the activity of methylase in the cells ( < 0.05).
CONCLUSIONS
Luteolin inhibits the proliferation of MDA-MB-231 breast cancer cells probably by upregulating OPCML expression and its demethylation.
Apoptosis
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Breast Neoplasms
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Cell Adhesion Molecules
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Cell Line, Tumor
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Cell Proliferation
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GPI-Linked Proteins
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Humans
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Luteolin