Fucosyltransferase-producing sialyl Lea and sialyl Lex carbohydrate antigen in benign and malignant gastrointestinal mucosa

Dohi, Taeko; Hashiguchi, Mitsuko; Yamamoto, Shigeru; Morita, H.; Oshima, Mieko

doi:10.1002/1097-0142(19940315)73:6<1552::aid-cncr2820730605>3.0.co;2-6

Cited by 40 publications

(23 citation statements)

References 19 publications

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“…This is demonstrated, for example, by the occurrence of abnormal synthesis of mucus glycoproteins [Lewis blood groups, Ca 19-9, sialyl Le(x)], and unexpected expression of abnormal gene products (K-ras) in gastritic stomach or intestinal metaplasia without any evidence of coexist, overt precancerous lesions, such as dysplasia or adenoma. [5][6][7][8][9][10][11] It seems plausible that an array of various genotoxic affections are triggered by the H. pylori gastritis, and that the resulting gene errors may play a role as effector mechanisms modulating the further course and outcomes of the H. pylori acquisition. Correspondingly, it is possible that even atrophic gastritis may result from unknown mutations in epithelial cell genes and may, thereby, stem from an imbalance between abnormal proliferation and death (apoptosis) of the epithelial cells.…”

Section: Discussionsupporting

confidence: 78%

Pathogenesis of the transformation from gastritis to malignancy

Sipponen¹,

Hyvärinen

Seppälä

et al. 1998

Aliment Pharmacol Ther

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cause of chronic gastritis, and on the knowledge of the natural course of chronic gastritis from non-atrophic gastritis to atrophic gastritis and intestinal metaplasia, and to precancerous lesions ( Figure 1). Prospective cohort studies are also considered to indicate strongly an association of H. pylori infection with gastric cancer. 1Our knowledge of the global epidemiology and time trends of gastric cancer indicates the importance of environmental factors in cancer pathogenesis. The timerelated changes in gastric cancer incidence have been substantial over the years but these changes are surprisingly similar worldwide, suggesting that one or some environmental agents play a critical role globally in gastric carcinogenesis.

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Section: Discussionsupporting

confidence: 78%

Pathogenesis of the transformation from gastritis to malignancy

Sipponen¹,

Hyvärinen

Seppälä

et al. 1998

Aliment Pharmacol Ther

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“…The reaction mixture contained 25 mM HEPES (pH 7.2), 20 mM MnCl 2 , 0.45% Triton CF54, 0.04 mM oligosaccharide-aminopyridine, 2 mM GDP-fucose, 5 mM CDP-choline, and 200 g of protein in a volume of 0.05 ml (27).…”

Section: Methodsmentioning

confidence: 99%

Suppression of Sialyl Lewis X Expression and E-selectin-mediated Cell Adhesion in Cultured Human Lymphoid Cells by Transfection of Antisense cDNA of an α1→3 Fucosyltransferase (Fuc-T VII)

Hiraiwa

Dohi

Kawakami-Kimura

et al. 1996

Journal of Biological Chemistry

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The antisense cDNA approach was used to identify the endogenous fucosyltransferase species responsible for synthesis of the sialyl Lewis X (NeuAc␣233 Gal␤134[Fuc␣133]GlcNAc␤13 R) determinant in human lymphoid cells. The cultured human adult T-cell leukemia cell line, ED40515-N, expressed the message of ␣133 fucosyltransferase (Fuc-T) IV and VII, with a low level of the Fuc-T III and VI message, and manifested the sialyl Lewis X as well as Lewis X (Gal␤134 [Fuc␣133]GlcNAc␤13 R) determinant at the cell surface. Transfection of this cell line with the pRc/CMV vector containing an antisense human Fuc-T VII construct (pRc/CMV/5FT7AS) resulted in a significant decrease of endogenous Fuc-T VII message and a marked reduction in the cell surface expression of sialyl Lewis X determinant as well as a reduction in the enzymatic activity of ␣133 fucosyltransferase against sialylated type 2 chain substrate. This was accompanied by diminution of cell adhesive activity toward E-selectin on interleukin-1␤-treated endothelial cells. These results indicated that the synthesis of the sialyl Lewis X determinants that were functionally active as E-selectin ligands was mainly mediated by Fuc-T VII in these lymphoid cells. On the other hand, the message of Fuc-T IV showed no significant change in the transfectant clones, and the surface expression of the Lewis X antigen as well as the enzymatic activity of ␣133 fucosyltransferase against non-sialylated type 2 chain substrate was well preserved. The clear contrast between the diminished expression of sialyl Lewis X and the conserved manifestation of Lewis X in the transfectant clones suggested that the synthesis of sialyl Lewis X and that of Lewis X are independently regulated by different fucosyltransferases in human lymphoid cells. Fuc-T VII must be involved in the synthesis of sialyl Lewis X, while the synthesis of Lewis X is mediated by an enzyme other than Fuc-T VII, most probably Fuc-T IV.

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“…15-18 Our preliminary studies indicated that sLeX, a glycan which binds with strong affinity to the E-selectin, facilitates HNSCC binding to EC under conditions of flow. 19,20 Expression of sLeX has been observed in several human malignancies, including HNSCC, and circulating levels of sLeX positive tumor cells were reported to be predictive for metastasis in GI carcinomas.…”

Section: Introductionmentioning

confidence: 93%

In vitro Evaluation of Sialyl Lewis X Relationship with Head and Neck Cancer Stem Cells

Czerwinski

Desiderio

Shkeir

et al. 2013

Otolaryngol.--head neck surg.

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Objective To evaluate in vitro the potential links between sialyl Lewis X (sLeX) and cancer stem cells (CSC) in head and neck squamous cell carcinoma (HNSCC). HNSCC is an aggressive malignancy with high mortality mainly due to metastasis. CSC have emerged as important players in HNSCC metastasis. sLeX is a tetrasaccharide carbohydrate known to play a key-role in metastatic dissemination by promoting binding of the tumor cells to the endothelium. Study Design Experimental, in vitro. Setting Laboratory of Head and Neck Cancer Metastasis, University of Michigan. Subjects and Methods A panel of stage- and anatomic-site specific primary and metastatic HNSCC cell lines was assessed by flow cytometry to quantify sLeX relative expression levels. Serum-free conditioned media from the same HNSCC lines was collected over a time-course of 72 hours and assessed by Western-blot for secreted sLeX expression. Representative HNSCC cell lines were cultured as floating orospheres (condition that enhance CSC growth) or under normal adherent conditions and characterized by flow cytometry for CSC markers (CD44, aldehyde dehydrogenase [ALDH]) comparatively with sLeX expression. Results sLeX is predominantly expressed in carcinomas originating from the oral cavity. Secreted sLeX is also found to be high in oral carcinomas and increased over the analyzed time course. Floating orospheres were strongly positive for CD44 and ALDH confirming CSC enrichment of the orospheres. Tumor cells grown as orospheres are 95-100% positive for sLeX compared to 10-40% of adherent counterpart. Conclusion These studies provide the first evidence of sLeX relationship with CSC in HNSCC.

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Fucosyltransferase-producing sialyl Lea and sialyl Lex carbohydrate antigen in benign and malignant gastrointestinal mucosa

Cited by 40 publications

References 19 publications

Pathogenesis of the transformation from gastritis to malignancy

Pathogenesis of the transformation from gastritis to malignancy

Suppression of Sialyl Lewis X Expression and E-selectin-mediated Cell Adhesion in Cultured Human Lymphoid Cells by Transfection of Antisense cDNA of an α1→3 Fucosyltransferase (Fuc-T VII)

In vitro Evaluation of Sialyl Lewis X Relationship with Head and Neck Cancer Stem Cells

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