scholarly journals Sialyl Lewis(a): a tumor-associated carbohydrate antigen involved in adhesion and metastatic potential of cancer cells.

2002 ◽  
Vol 49 (2) ◽  
pp. 303-311 ◽  
Author(s):  
Maciej Ugorski ◽  
Anna Laskowska
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Human Cancer ◽  
Metastatic Potential ◽  
Sialyl Lewis X ◽  
Adhesion Assay ◽  
Sialyl Lewis ◽  
Sialyl Lewis A ◽  
Lewis A

Neoplastic transformation is often associated with characteristic changes in the expression of the sialyl Lewis(a) and sialyl Lewis(x) antigens, representing typical tumor-associated carbohydrate antigens. High amounts of sialyl Lewis(a) are present in human adenocarcinomas of the colon, pancreas and stomach. A growing amount of data suggests that this carbohydrate structure is the ligand for E-selectin. Sialylated Lewis structures present on the surface of tumor cells are carried by the carbohydrate chains of glycoproteins and glycolipids. There are several lines of evidence showing that sialyl Lewis(a) is responsible for the adhesion of human cancer cells to endothelium. E-selectin present on endothelial cells mediates these interactions. Selectins and their carbohydrate ligands can thus play an important role in the selective homing of tumor cells during metastasis. However, the presence of sialyl Lewis(a) antigen on the surface of tumor cells and their adhesion to E-selectin-expressing cells in in vitro adhesion assay by itself can not be directly related to metastatic properties of all cancer cells.

scholarly journals De novo expression of endothelial sialyl Lewis(a) and sialyl Lewis(x) during cardiac transplant rejection: superior capacity of a tetravalent sialyl Lewis(x) oligosaccharide in inhibiting L-selectin-dependent lymphocyte adhesion.

1995 ◽  
Vol 182 (4) ◽  
pp. 1133-1141 ◽  
Author(s):  
J P Turunen ◽  
M L Majuri ◽  
A Seppo ◽  
S Tiisala ◽  
T Paavonen ◽  
...  
Keyword(s):  
De Novo ◽  
Transplant Rejection ◽  
Sialyl Lewis X ◽  
Cardiac Transplant ◽  
Lewis X ◽  
Lymphocyte Adhesion ◽  
Sialyl Lewis ◽  
Sialyl Lewis A ◽  
Lewis A

Acute organ transplant rejection is characterized by a heavy lymphocyte infiltration. We have previously shown that alterations in the graft endothelium lead to increased lymphocyte traffic into the graft. Here, we demonstrate that lymphocytes adhere to the endothelium of rejecting cardiac transplants, but not to the endothelium of syngeneic grafts or normal hearts analyzed with the in vitro Stamper-Woodruff binding assay. Concomitant with the enhanced lymphocyte adhesion, the cardiac endothelium begins to de novo express sialyl Lewis(a) and sialyl Lewis(x) (sLea and sLex) epitopes, which have been shown to be sequences of L-selectin counterreceptors. The endothelium of allografts, but not that of syngeneic grafts or normal controls, also reacted with the L-selectin-immunoglobulin G fusion protein, giving further proof of inducible L-selectin counterreceptors. The lymphocyte adhesion to endothelium could be significantly decreased either by treating the lymphocytes with anti-L-selectin antibody HRL-1, or by treating the tissue sections with sialidase or anti-sLea or anti-sLex monoclonal antibodies. Finally, we synthetized enzymatically several members of the sLex family oligosaccharides and analyzed their ability to block lymphocyte adhesion to cardiac endothelium. The monovalent sLex (a tetramer), divalent sLex (a decamer), and tetravalent sLex (a 22-mer) could all significantly reduce lymphocyte binding, but the inhibition by the tetravalent sLex-construct was clearly superior to other members of the sLex family. The crucial control oligosaccharides, sialyl lactosamines lacking fucose but being otherwise similar to the members of sLex family, had no effect on lymphocyte binding.

Adhesion of human cancer cells to vascular endothelium mediated by a carbohydrate antigen, sialyl Lewis A

1991 ◽  
Vol 179 (2) ◽  
pp. 713-719 ◽  
Author(s):  
Akiko Takada ◽  
Katsuyuki Ohmori ◽  
Naofumi Takahashi ◽  
Kiyotaka Tsuyuoka ◽  
Akihiro Yago ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Vascular Endothelium ◽  
Human Cancer ◽  
Carbohydrate Antigen ◽  
Human Cancer Cells ◽  
Sialyl Lewis ◽  
Sialyl Lewis A ◽  
Lewis A

Significance of Carbohydrate Antigen Sialyl-Lewis X, Sialyl-Lewis A, and Possible Unknown Ligands to Adhesion of Human Urothelial Cancer Cells to Activated Endothelium

2000 ◽  
Vol 64 (3) ◽  
pp. 129-133 ◽  
Author(s):  
Yasuhisa Fujii ◽  
Masayuki Yoshida ◽  
Lee-Jung Chien ◽  
Kazunori Kihara ◽  
Yukio Kageyama ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Urothelial Cancer ◽  
Carbohydrate Antigen ◽  
Sialyl Lewis X ◽  
Lewis X ◽  
Sialyl Lewis ◽  
Sialyl Lewis A ◽  
Lewis A

scholarly journals Selectin Ligands Sialyl-Lewis a and Sialyl-Lewis x in Gastrointestinal Cancers

Biology ◽  
2017 ◽  
Vol 6 (4) ◽  
pp. 16 ◽  
Author(s):  
Marco Trinchera ◽  
Adele Aronica ◽  
Fabio Dall’Olio
Keyword(s):  
Sialyl Lewis X ◽  
Gastrointestinal Cancers ◽  
Lewis X ◽  
Sialyl Lewis ◽  
Selectin Ligands ◽  
Sialyl Lewis A ◽  
Lewis A

scholarly journals Repression of LKB1 by miR-17∼92 sensitizes MYC-dependent lymphoma to biguanide treatment

2019 ◽  
Author(s):  
Said Izreig ◽  
Alexandra Gariepy ◽  
Ariel O. Donayo ◽  
Gaëlle Bridon ◽  
Daina Avizonis ◽  
...  
Keyword(s):  
Cancer Cells ◽  
Tumor Cells ◽  
Human Cancer ◽  
Tca Cycle ◽  
Mirna Cluster ◽  
Lymphoma Cells ◽  
Ampk Signaling ◽  
Potential Biomarker

AbstractCancer cells display metabolic plasticity to survive metabolic and energetic stresses in the tumor microenvironment, prompting the need for tools to target tumor metabolism. Cellular adaptation to energetic stress is coordinated in part by signaling through the Liver Kinase B1 (LKB1)-AMP-activated protein kinase (AMPK) pathway. Reducing LKB1-AMPK signaling exposes metabolic vulnerabilities in tumor cells with potential for therapeutic targeting. Here we describe that miRNA-mediated silencing of LKB1 (mediated by the oncogenic miRNA cluster miR-17∼92) confers sensitivity of lymphoma cells to mitochondrial inhibition by biguanides. Using both classic (phenformin) and novel (IM156) biguanides, we demonstrate that Myc+ lymphoma cells with elevated miR-17∼92 expression display increased sensitivity to biguanide treatment both in cell viability assays in vitro and tumor growth assays in vivo. This increased biguanide sensitivity is driven by miR-17-dependent silencing of LKB1, which results in reduced AMPK activation in response to bioenergetic stress. Mechanistically, biguanide treatment inhibits TCA cycle metabolism and mitochondrial respiration in miR-17∼92-expressing tumor cells, targeting their metabolic vulnerability. Finally, we demonstrate a direct correlation between miR-17∼92 expression and biguanide sensitivity in human cancer cells. Our results identify miR-17∼92 expression as a potential biomarker for biguanide sensitivity in hematological malignancies and solid tumors.One Sentence SummarymiR-17∼92 expression in Myc+ tumors sensitizes cancer cells to biguanide treatment by disrupting bioenergetic stability in lymphoma cells.

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