Compare Anti-Glucose Transporter GLUT3 antibody ab from Abcam on Be the first to write a review! Rabbit polyclonal to Glucose Transporter GLUT3. C5 and T4 cells showed the highest rate of GLUT-3 expression. These cells were ORL J Otorhinolaryngol Relat Spec. ;– glucose transporter 3 (GLUT3)2 is the major GLUT subtype in .. platelets without additional Ca2 at 20 °C in a F fluorescence spec-.
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Additionally, liver cells commonly use Glut2 for glucose transportation. On respiratory impairment in cancer cells. Expression and localization of Glut1 and Glut 12 glucose transporters in the pregnant and lactating rat mammary gland. Transformed cells were seeded onto Matrigel invasion chambers and at the end of a h incubation period.
Gluy3 has been well known that prolonged estrogenic exposure, such as early menarche, late menopause or hormone replacement therapy, have been considered main risk factors for the development of human breast cancer [ 2627 ]. Glut3 had an increase in gene expression in all the cells derived from MCF10F. Under the hypoxic conditions, oncogenic signals activate a transcription g,ut3 HIF-1 complex that controls the cellular adaptation of transformed glur3 to low oxygen.
Glut-1 antibodies induce growth arrest and apoptosis gltu3 human cancer cell lines. Growth factor signalling networks in the breast cancer and resistance to endocrine agents: In the present study, we aimed to investigate the expression patterns of three GLUT isoforms in the E2-induced in vitro mammary carcinogenesis model.
On the other hand, quite a few data have been published about the role of estrogens on Glut3 expression in tumoral cell lines. Glucose avidity of carcinomas.
We have previously postulated that differentiation of mammary gland determines the susceptibility to carcinogenesis [ 53 ]. Functional properties and genomics of glucose transporters. Although increased glucose metabolism and overexpression of Gluts in cancer are well known, reasons for tumor and stage-specific alterations as seen at Fig.
This hormone is also particularly effective in further stages, for example acceleration of the cellular growth and progression of the premalignant xenografts [ 31 ]. Concordant with this suggestion, Rivenzon-Segal and co-workers [ 55 ] have found that differentiation of the breast cancer cell line T47D with retinoic acid led to a reduction in Glut-1 and to an increase in cytoplasmic Glut-3 as well as decreased glycolysis.
Cellular adaptations to hypoxia and acidosis during somatic evaluation of breast cancer. Tumor hypoxia, another hallmark of malignant progression, up-regulates glucose transporter proteins.
Similar results can be obtained using Glut-3 antibodies or Glut-3 modulation methods in our model system. Here, we have demonstrated for the first time that estrogen-induced malignant progression is associated with progressive Glut3 over-expression.
For example, E2-transformed cells exhibited LOH in chromosomes 3 and 11, glur3 BP did not induce genomic changes during the same period of time. Author manuscript; available in PMC Aug 1. Kinase-specific phosphorylation of the estrogen receptor changes receptor interactions with ligand, deoxyribonucleic acid, and coregulators associated with alterations in estrogen and tamoxifen activity. National Center for Biotechnology InformationU.
Similar to E2 cells, BP1-Tras and MDA-MB exhibited a complete absence of ductule formation, forming instead solid masses in collagen whose values were not significantly different from those formed by E2-induced cells. The all comparisons were significant.
So far, 14 different GLUT isoforms are established and classified. For example, Young and co-workers have shown that modulation of Glut1 expression levels alters mouse mammary tumor cell growth in the in vivo and in vitro conditions [ 70 gljt3.
For example, loss of 9p, LOH D13S, Delp53 exon4, persisted in all transformed cells; complete loss of chromosome 4 was observed in C5 and T4 cells.
Shi J, Simpkins JW.
Expression analyses of the other isoforms in tumor tissues appeared less consistent. Kocdor2 J. Two-tailed unpaired t test was used for gene expression analysis. In addition, it has been shown that estrogen plays critical roles in GLUT regulation, however, the stage-specific GLUT regulation of mammary carcinogenesis is unclear. We used our glutt3 vitro—in vivo progressive mammary carcinogenesis model which consisted of 4 cell lines, from healthy MCFF to tumorigenic cells E2, C5, T4with the same genetic background Fig.
GLUT – The OpenGL Utility Toolkit
Biochem Biophy Res Commun. In order to mimic the intermittent exposure of MCF10F to endogenous estrogens, cells were first treated with physiological doses of E2 at 72 and h post-plating.
Three-dimensional growth in type 1 collagen matrix: The glycolytic phenotype or Warburg effect is not only associated with excessive glucose consumption by overexpression of different Glut isoforms, but also increased activity of enzymes involved in glycolysis [ 58 ].
Neeman M, Degani H. Solute carrier family 2 facilitated glucose transportermember Our laboratory previously demonstrated that short-term 2 weeks treatment of MCFF cells with estradiol and its catechol metabolites induce these phenotypes indicative of neoplastic transformation [ 3039 ]. It is well known that the members of EGFR family play important role in regulating a number of cellular processes, differentiation and malignant transformation [ 61 ]. In addition, the comparison between C5 and T4 groups was statistically significant.
Therefore, we believe that the present model is more appropriate with regard to testing stage-specific gene expression profiles under the influence of estrogenic action. The expression is shown in fold change related to MCF10F cells.
Causes and consequences of increased glucose metabolism of cancers.