Pentaspan membrane glycoprotein, prominin-1, is involved in glucose metabolism and cytoskeleton alteration

Yang, Chang; Yang, Yanli; Gupta, Nishith; Liu, Xiaojun; He, Aibin; Liu, Lizhong; Zuo, Jun; Chang, Yongsheng; Fang, Fude

doi:10.1134/s000629790708007x

Cited by 7 publications

(8 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Supporting the aerobic glycolysis of cancer cells first reported by Otto Warburg in the 1950s [68], it was recently established that CD133 expression is associated with high cellular glucose metabolism: CD133 was found to be a glucose responsive gene in L6 myotubes [11] and CD133 expression to be concomitant to high glucose cellular uptake in U251 glioma cells [12]. Since co-localization of glucose transporters with the TfR in intracellular vesicles has previously been observed [69], [70], [71], whether CD133 can regulate iron uptake together with glucose transport by modulation of endocytosis remains an important question.…”

Section: Discussionmentioning

confidence: 82%

“…In addition, AC133, a glycosylated epitope of CD133 protein initially associated with embryonic stem cells [8] and a variety of somatic stem cells, was extensively described as a putative cancer stem cell marker in blood, brain, colon, prostate, lung, breast, liver, and skin cancers [9], [10]. Other investigations revealed that CD133 is linked to cell metabolism as a glucose responsive gene in myotubes [11], as well as providing evidence for bioenergetic stress [12] and of non-exposure to high oxygen tension in gliomas (Bourseau-Guilmain et al, submitted).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The Importance of the Stem Cell Marker Prominin-1/CD133 in the Uptake of Transferrin and in Iron Metabolism in Human Colon Cancer Caco-2 Cells

et al. 2011

View full text Add to dashboard Cite

As the pentaspan stem cell marker CD133 was shown to bind cholesterol and to localize in plasma membrane protrusions, we investigated a possible function for CD133 in endocytosis. Using the CD133 siRNA knockdown strategy and non-differentiated human colon cancer Caco-2 cells that constitutively over-expressed CD133, we provide for the first time direct evidence for a role of CD133 in the intracellular accumulation of fluorescently labeled extracellular compounds. Assessed using AC133 monoclonal antibody, CD133 knockdown was shown to improve Alexa488-transferrin (Tf) uptake in Caco-2 cells but had no impact on FITC-dextran or FITC-cholera-toxin. Absence of effect of the CD133 knockdown on Tf recycling established a role for CD133 in inhibiting Tf endocytosis rather than in stimulating Tf exocytosis. Use of previously identified inhibitors of known endocytic pathways and the positive impact of CD133 knockdown on cellular uptake of clathrin-endocytosed synthetic lipid nanocapsules supported that CD133 impact on endocytosis was primarily ascribed to the clathrin pathway. Also, cholesterol extraction with methyl-β-cyclodextrine up regulated Tf uptake at greater intensity in the CD133high situation than in the CD133low situation, thus suggesting a role for cholesterol in the inhibitory effect of CD133 on endocytosis. Interestingly, cell treatment with the AC133 antibody down regulated Tf uptake, thus demonstrating that direct extracellular binding to CD133 could affect endocytosis. Moreover, flow cytometry and confocal microscopy established that down regulation of CD133 improved the accessibility to the TfR from the extracellular space, providing a mechanism by which CD133 inhibited Tf uptake. As Tf is involved in supplying iron to the cell, effects of iron supplementation and deprivation on CD133/AC133 expression were investigated. Both demonstrated a dose-dependent down regulation here discussed to the light of transcriptional and post-transciptional effects. Taken together, these data extend our knowledge of the function of CD133 and underline the interest of further exploring the CD133-Tf-iron network.

show abstract

Section: Discussionmentioning

confidence: 82%

Section: Introductionmentioning

confidence: 99%

The Importance of the Stem Cell Marker Prominin-1/CD133 in the Uptake of Transferrin and in Iron Metabolism in Human Colon Cancer Caco-2 Cells

et al. 2011

View full text Add to dashboard Cite

show abstract

“…In fact, in a conditional ablation model, tamoxifen-induced ablation of Prom1-expressing cells caused body weight loss ( 9 ). Studies have pointed to the potential involvement of Prom1 in cellular metabolism in rat myotubes and mouse pancreatic islets with contrasting findings ( 29 , 30 ), and an increase in Prom1 expression in young mice with induced obesity has been reported ( 31 ). In other respects, PROM1 was shown to promote glucose uptake in a human hepatocellular carcinoma cell line ( 32 ).…”

mentioning

confidence: 99%

Commentary: “Prom1 Function in Development, Intestinal Inflammation, and Intestinal Tumorigenesis”

2015

View full text Add to dashboard Cite

“…These results support the findings of other authors such as Immervoll et al (24), whose data indicated that CD133 is involved in cellular polarity and is required for cellular movement as well as the processes of chemotaxis, embryonic development, invasive growth and metastasis. In addition, Yang et al (25) reported CD133 involvement in glucose metabolism and cytoskeleton alteration. Additionally, Rappa et al (7) showed that the downregulation of CD133 resulted in retarded cell growth, reduced cell motility and a decreased ability to form spheroids under stem cell-like growth conditions.…”

Section: Discussionmentioning

confidence: 99%

CD133 antisense suppresses cancer cell growth and increases sensitivity to cisplatin in vitro

Blancas-Mosqueda

Zapata‐Benavides

Zamora-Ávila

et al. 2012

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

The increased incidence of cancer in recent years is associated with a high rate of mortality. Numerous types of cancer have a low percentage of CD133+ cells, which have similar features to stem cells. The CD133 molecule is involved in apoptosis and cell proliferation. The aim of this study was to determine the biological effect of CD133 suppression and its role in the chemosensitization of cancer cell lines. RT-PCR and immunocytochemical analyses indicated that CD133 was expressed in the cancer cell lines B16F10, MCF7 and INER51. Downregulation of CD133 by transfection with an antisense sequence (As-CD133) resulted in a decrease in cancer cell viability of up to 52, 47 and 22% in B16F10, MCF-7 and INER51 cancer cell lines, respectively. This decreased viability appeared to be due to the induction of apoptosis. In addition, treatment with As-CD133 in combination with cisplatin had a synergic effect in all of the cancer cell lines analyzed, and in particular, significantly decreased the viability of B16F10 cancer cells compared with each treatment separately (3.1% viability for the combined treatment compared with 48% for 0.4 μg As-CD133 and 25% for 5 ng/μl cisplatin; P<0.05). The results indicate that the downregulation of CD133 by antisense is a potential therapeutic target for cancer and has a synergistic effect when administered with minimal doses of the chemotherapeutic drug cisplatin, suggesting that this combination strategy may be applied in cancer treatment.

show abstract

Pentaspan membrane glycoprotein, prominin-1, is involved in glucose metabolism and cytoskeleton alteration

Cited by 7 publications

References 27 publications

The Importance of the Stem Cell Marker Prominin-1/CD133 in the Uptake of Transferrin and in Iron Metabolism in Human Colon Cancer Caco-2 Cells

The Importance of the Stem Cell Marker Prominin-1/CD133 in the Uptake of Transferrin and in Iron Metabolism in Human Colon Cancer Caco-2 Cells

Commentary: “Prom1 Function in Development, Intestinal Inflammation, and Intestinal Tumorigenesis”

CD133 antisense suppresses cancer cell growth and increases sensitivity to cisplatin in vitro

Contact Info

Product

Resources

About