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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Tumor hypoxia, another hallmark of malignant progression, up-regulates glucose transporter proteins. Microenvironmental regulation of estrogen signals in breast cancer.
Cancer cells, similar to non-tumoral mammalian cells, utilize glucose as main energy substrate using only these facilitative transport systems GLUTs depending on their increased metabolic activity and rapid proliferation [ 34 ]. Ductulogenic xpec and solid mass formation were evaluated as previously described [ 2830 ].
Schematic presentation of the previous experimental protocol and genomic characteristics of the cell lines used are summarized in Fig. Molecular and cellular regulation of glucose transporter Glut proteins in cancer.
In other series, Glut3 expression is relatively high in aggressive tumors including breast, choriocarcinoma and lung tumors [ 410 ]. In our previous studies, transforming potential of E2 on MCF10F was compared with chemical carcinogen benzo[a]pyrene BP by using the same in vitro model.
Other analyses were performed using statistical software and differences were further evaluated using Holm—Sidak test for multiple pair-wise gut3 procedures SigmaStat 3.
Mean colony number in C5 group was statistically higher than T4 Student t test. After treatment with E2, MCFF cells almost completely lost their ductulogenic capacity, while acquired solid mass formation in collagen.
Especially within the last decade, expression patterns of GLUT isoforms mostly Glut1—5 have been gluf3 in several tumor cell lines and tumor tissue specimens [ 4 ].
J Steroid Biochem Mol Biol. Modulation of glucose transporter1 Glut1 expression levels alters Mouse mammary tumor cell growth in vitro and in vivo. Estrogen and its metabolites are carcinogenic agents in human breast epithelial cells. J Mammary Gland Biol Neoplasia.
For example, malignant transformation of Rat1 fibroblasts with H-ras results in a substantial increase in glut1 mRNA levels in hypoxic conditions and thus, H-ras may specifically up-regulate Glut1 promoter [ 44 ]. However, Godoy et al.
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Airley RE, Mobasheri A. Similar results can be obtained using Glut-3 antibodies or Glut-3 modulation methods in glur3 model system. In this model, different stages of tumor initiation and progression are represented, MCFF being the normal stage, E2 cells the transformed stage by estrogen, C5 cells, the invasive stage, and T4 cells the tumorigenic stage.
National Center for Biotechnology InformationU. The concept of stem cell in mammary gland and its implication in morphogenesis, cancer and prevention. Breast tumor tissue specimens and cultured breast carcinoma cells are often associated with the overexpression of Gluts, particularly Glut1 and less frequently Glut3 [ 410 ].
However, when this cell line is subjected to carcinogenic exposure i. 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. Louis, MO, USA or DMSO control for h periods twice a week for 2 weeks; 24 h after the last treatment the cells were soec and maintained in culture for ten additional passages.
The role of estrogen in the initiation of breast cancer. Regulation of mammary gland development and tumorigenesis by the ERBB signalling network. Colony formation of represented cells in Agar methocel right column. ylut3
Hypoxia reduces hormone responsiveness of human breast cancer cells. Expression and localization of Glut1 and Glut 12 glucose transporters in the pregnant and lactating rat mammary gland.
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Spwc and progesterone up-regulate glucose transporter expression in ZR human breast cancer cells. Epithelial to mesenchymal transition in human breast epithelial cells transformed by 17beta-estradiol. Glucose avidity of carcinomas. These cells were also found to be associated with loss of ductulogenesis, solid mass formation and higher invasive capacity, whereas, GLUT was downregulated in C5 and T4 cells. A family of glucose transporters GLUTs facilitates glucose movement across the plasma membranes in a tumor-specific manner.