scholarly journals METCAM/MUC18 Promotes Tumor Progression and Metastasis in Most Human Cancers

2020 ◽  
Author(s):  
Guang-Jer Wu
Keyword(s):  
Tumor Progression ◽  
Human Cancers

scholarly journals The Embryonic Key Pluripotent Factor NANOG Mediates Glioblastoma Cell Migration via the SDF1/CXCR4 Pathway

2021 ◽  
Vol 22 (19) ◽  
pp. 10620
Author(s):  
Ana Virginia Sánchez-Sánchez ◽  
Antonio García-España ◽  
Pilar Sánchez-Gómez ◽  
Jaime Font-de-Mora ◽  
Marián Merino ◽  
...  
Keyword(s):  
Cell Migration ◽  
Tumor Progression ◽  
Cancer Cell ◽  
Embryonic Stem ◽  
Regulatory Elements ◽  
Cellular Migration ◽  
Cancer Cell Migration ◽  
Medaka Fish ◽  
Human Cancers ◽  
Nanog Expression

NANOG is a key transcription factor required for maintaining pluripotency of embryonic stem cells. Elevated NANOG expression levels have been reported in many types of human cancers, including lung, oral, prostate, stomach, breast, and brain. Several studies reported the correlation between NANOG expression and tumor metastasis, revealing itself as a powerful biomarker of poor prognosis. However, how NANOG regulates tumor progression is still not known. We previously showed in medaka fish that Nanog regulates primordial germ cell migration through Cxcr4b, a chemokine receptor known for its ability to promote migration and metastasis in human cancers. Therefore, we investigated the role of human NANOG in CXCR4-mediated cancer cell migration. Of note, we found that NANOG regulatory elements in the CXCR4 promoter are functionally conserved in medaka fish and humans, suggesting an evolutionary conserved regulatory axis. Moreover, CXCR4 expression requires NANOG in human glioblastoma cells. In addition, transwell assays demonstrated that NANOG regulates cancer cell migration through the SDF1/CXCR4 pathway. Altogether, our results uncover NANOG-CXCR4 as a novel pathway controlling cellular migration and support Nanog as a potential therapeutic target in the treatment of Nanog-dependent tumor progression.

scholarly journals Fucosylated Glycoproteins as Markers of Liver Disease

2008 ◽  
Vol 25 (4-5) ◽  
pp. 259-265 ◽  
Author(s):  
Anand Mehta ◽  
Timothy M. Block
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Disease ◽  
Liver Fibrosis ◽  
Tumor Progression ◽  
Cancer Metastasis ◽  
Total Serum ◽  
Human Cancers ◽  
Specific Igg ◽  
Core Fucosylation

Changes in N-linked glycosylation are known to occur during the development of various diseases. For example, increased branching of oligosaccharides has been associated with cancer metastasis and has been correlated to tumor progression in human cancers of the breast, colon and melanomas. Increases in core fucosylation have also been associated with the development of hepatocellular carcinoma (HCC). Recently, changes in both the total serum glycome and the glycosylation of specific IgG molecules have been observed in people with liver fibrosis and cirrhosis. The mechanisms by which changes in glycosylation are observed and their use as biomarkers of disease will be discussed.

scholarly journals YAP/TAZ Activation as a Target for Treating Metastatic Cancer

Cancers ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 115 ◽  
Author(s):  
Janine Warren ◽  
Yuxuan Xiao ◽  
John Lamar
Keyword(s):  
Tumor Progression ◽  
Experimental Evidence ◽  
Cancer Progression ◽  
Metastatic Disease ◽  
Metastatic Cancer ◽  
Causal Role ◽  
Binding Motif ◽  
Metastatic Cascade ◽  
Human Cancers ◽  
Promising Strategy

Yes-Associated Protein (YAP) and Transcriptional Co-activator with PDZ-binding Motif (TAZ) have both emerged as important drivers of cancer progression and metastasis. YAP and TAZ are often upregulated or nuclear localized in aggressive human cancers. There is abundant experimental evidence demonstrating that YAP or TAZ activation promotes cancer formation, tumor progression, and metastasis. In this review we summarize the evidence linking YAP/TAZ activation to metastasis, and discuss the roles of YAP and TAZ during each step of the metastatic cascade. Collectively, this evidence strongly suggests that inappropriate YAP or TAZ activity plays a causal role in cancer, and that targeting aberrant YAP/TAZ activation is a promising strategy for the treatment of metastatic disease. To this end, we also discuss several potential strategies for inhibiting YAP/TAZ activation in cancer and the challenges each strategy poses.

Expressions of cyclooxygenase-2 (COX-2) and prostaglandin E receptors (EPs) in gallbladder carcinoma (GBca)-association with tumor progression

2001 ◽  
Vol 120 (5) ◽  
pp. A573-A573
Author(s):  
J SHODA ◽  
T ASANO ◽  
T KAWAMOTO ◽  
Y MATSUZAKI ◽  
N TANAKA ◽  
...  
Keyword(s):  
Tumor Progression ◽  
Gallbladder Carcinoma ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Cox 2

150: Inhibition of Tumor Progression Using Antisense Oligonucleotide Targeting GLI2 in Androgen Independent Prostate Cancer

2007 ◽  
Vol 177 (4S) ◽  
pp. 51-51
Author(s):  
Shintaro Narita ◽  
Alan I. So ◽  
Shannon Sinnemann ◽  
Ladan Fazli ◽  
Eric G. Marcusson ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Tumor Progression ◽  
Antisense Oligonucleotide ◽  
Androgen Independent

THE ROLE OF TGFΒ IN HUMAN CANCERS

Pathology ◽  
2001 ◽  
Vol 33 (1) ◽  
pp. 85-92 ◽  
Author(s):  
Shew-Fung Wong, Leslie C. Lai
Keyword(s):  
Human Cancers
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