Hypoxia, Angiogenesis, and Oral Cancer Metastasis

2009 ◽  
pp. 299-321 ◽  
Author(s):  
Quynh-Thu Le ◽  
Donald Courter ◽  
Amato Giaccia
Keyword(s):  
Oral Cancer ◽  
Cancer Metastasis

scholarly journals Caffeic Acid Phenethyl Ester Inhibits Oral Cancer Cell Metastasis by Regulating Matrix Metalloproteinase-2 and the Mitogen-Activated Protein Kinase Pathway

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Chih-Yu Peng ◽  
Hui-Wen Yang ◽  
Yin-Hung Chu ◽  
Yu-Chao Chang ◽  
Ming-Ju Hsieh ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Matrix Metalloproteinase ◽  
Caffeic Acid ◽  
Cancer Cell ◽  
Cancer Metastasis ◽  
Caffeic Acid Phenethyl Ester ◽  
Matrix Metalloproteinase 2 ◽  
Migration And Invasion ◽  
Oral Cancer Cell ◽  
Cell Metastasis

Caffeic acid phenethyl ester (CAPE), an active component extracted from honeybee hives, exhibits anti-inflammatory and anticancer activities. However, the molecular mechanism by which CAPE affects oral cancer cell metastasis has yet to be elucidated. In this study, we investigated the potential mechanisms underlying the effects of CAPE on the invasive ability of SCC-9 oral cancer cells. Results showed that CAPE attenuated SCC-9 cell migration and invasion at noncytotoxic concentrations (0 μM to 40 μM). Western blot and gelatin zymography analysis findings further indicated that CAPE downregulated matrix metalloproteinase-2 (MMP-2) protein expression and inhibited its enzymatic activity. CAPE exerted its inhibitory effects on MMP-2 expression and activity by upregulating tissue inhibitor of metalloproteinase-2 (TIMP-2) and potently decreased migration by reducing focal adhesion kinase (FAK) phosphorylation and the activation of its downstream signaling molecules p38/MAPK and JNK. These data indicate that CAPE could potentially be used as a chemoagent to prevent oral cancer metastasis.

Emerging concept of oral cancer metastasis induced from analysis of a cancer metastasis model

2015 ◽  
Vol 44 ◽  
pp. e263
Author(s):  
H. Miyashita ◽  
S. Mori ◽  
T. Kodama ◽  
T. Takahashi
Keyword(s):  
Oral Cancer ◽  
Cancer Metastasis ◽  
Metastasis Model

Role of Tumor Stromal Interactions and Proteases in Oral Cancer Metastasis

2009 ◽  
pp. 265-286
Author(s):  
J. Robert Newman ◽  
Eben L. Rosenthal
Keyword(s):  
Oral Cancer ◽  
Cancer Metastasis

scholarly journals Lipocalin 2 prevents oral cancer metastasis through carbonic anhydrase IX inhibition and is associated with favourable prognosis

2016 ◽  
Vol 37 (7) ◽  
pp. 712-722 ◽  
Author(s):  
Chiao-Wen Lin ◽  
Wei-En Yang ◽  
Wei-Jiunn Lee ◽  
Kuo-Tai Hua ◽  
Feng-Koo Hsieh ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Carbonic Anhydrase ◽  
Cancer Metastasis ◽  
Carbonic Anhydrase Ix ◽  
Lipocalin 2 ◽  
Favourable Prognosis

Predictive model of oral cancer metastasis for different cancer sites and age groups

2015 ◽  
Vol 7 (2) ◽  
pp. 127-131 ◽  
Author(s):  
Bogahawatte Samarakoon Mudiyanselag Siriwardena ◽  
Rasnayaka Mudiynaselage Sumudu Geet Rasnayaka ◽  
Yaghma Masood ◽  
Mohd Masood ◽  
Pallegoda Vithanage Ranjith Kumarasiri ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Predictive Model ◽  
Cancer Metastasis ◽  
Age Groups

Chemokines and Their Receptors in Oral Cancer Metastasis

2009 ◽  
pp. 287-298
Author(s):  
Yvonne K. Mburu ◽  
Robert L. Ferris
Keyword(s):  
Oral Cancer ◽  
Cancer Metastasis

scholarly journals Upregulation of LGALS1 is associated with oral cancer metastasis

2018 ◽  
Vol 10 ◽  
pp. 175883591879462 ◽  
Author(s):  
Ji-Min Li ◽  
Chien-Wei Tseng ◽  
Chi-Chen Lin ◽  
Ching-Hsuan Law ◽  
Yu-An Chien ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Cancer Metastasis ◽  
Mapk Pathway ◽  
Cancer Tissue ◽  
Mesenchymal Transition ◽  
Oral Cancer Cells

Background: Oral cancer metastasis is a devastating process that contributes to poor prognosis and high mortality, yet its detailed underlying mechanisms remain unclear. Here, we aimed to evaluate metastasis-specific markers in oral cancer and to provide comprehensive recognition concerning functional roles of the specific target in oral cancer metastasis. Methods: Lectin, galactoside-binding, soluble, 1 (LGALS1) was identified by secretomic analysis. LGALS1 expression of patient samples with oral cancer on the tissue microarray were examined by immunochemical (IHC) staining. Small interfering RNA (siRNA)-mediated knockdown of LGALS1 revealed the role of LGALS1 in oral cancer metastasis in vitro and in vivo. Results: LGALS1 was observed to be upregulated in highly invasive oral cancer cells, and elevated LGALS1 expression was correlated with cancer progression and lymph node metastasis in oral cancer tissue specimens. Functionally, silencing LGALS1 resulted in suppressed cell growth, wound healing, cell migration, and cell invasion in oral cancer cells in vitro. Knockdown of LGALS1 in highly invasive oral cancer cells dramatically inhibited lung metastasis in an in vivo mouse model. Mechanistic studies suggested p38 mitogen-activated protein kinase (MAPK) phosphorylation, upregulated MMP-9, and mesenchymal phenotypes of epithelial-mesenchymal transition (EMT) in highly invasive oral cancer cells, whereas siRNA against LGALS1 resulted in the inactivation of p38 MAPK pathway, downregulated MMP-9, and EMT inhibition. Conclusions: These findings demonstrate that elevated LGALS1 is strongly correlated with oral cancer progression and metastasis, and that it could potentially serve as a prognostic biomarker and an innovative target for oral cancer therapy.

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