Overexpression of CD133 promotes the phosphorylation of Erk in U87MG human glioblastoma cells
Research highlights
▶ CD133 is marker of cancer stem cell. ▶ P-Erk is significantly elevated in CD133+ cancer cells. ▶ Overexpression of CD133 promotes the phosphorylation of Erk in cancer cells.
Section snippets
Acknowledgements
We thank Dr. Sihai Ma (Department of Neurosurgery, Peking Union Medical College Hospital, Beijing, China) for technical assistance. We also would like to acknowledge Dr. Hamid Band (University of Nebraska Medical Center) for reading my revision of manuscript. This study was supported by grants from the Ministry of Science and Technology of China (2009ZX09103-733 and 2009ZX09301-010).
References (22)
- et al.
Counting on mitogen-activated protein kinases—ERKs 3, 4, 5, 6, 7 and 8
Cell Signal
(2004) - et al.
Analysis of gene expression and chemoresistance of CD133+ cancer stem cells in glioblastoma
Mol. Cancer
(2006) - et al.
MAP kinase modules: many roads home
Curr. Biol.
(2003) - et al.
Brain tumor stem cells: identification and concepts
Neurosurg. Clin. N. Am.
(2007) - et al.
Characterization of CD133+ hepatocellular carcinoma cells as cancer stem/progenitor cells
Biochem. Biophys. Res. Commun.
(2006) - et al.
The stem cell marker CD133 (prominin-1) is phosphorylated on cytoplasmic tyrosine-828 and tyrosine-852 by Src and Fyn tyrosine kinases
Biochemistry
(2009) - et al.
Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell
Nat. Med.
(1997) - et al.
Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses
Nature
(2010) - et al.
Prospective identification of tumorigenic prostate cancer stem cells
Cancer Res.
(2005) - et al.
CD133+ liver cancer stem cells from methionine adenosyl transferase 1A-deficient mice demonstrate resistance to transforming growth factor (TGF)-beta-induced apoptosis
Hepatology
(2009)
Identification and expansion of the tumorigenic lung cancer stem cell population
Cell Death Differ.
Cited by (22)
MicroRNA-377: A therapeutic and diagnostic tumor marker
2023, International Journal of Biological MacromoleculesCitation Excerpt :CD133 was investigated as one of the most commonly used markers to identify TICs [77]. CD133 induced TIC or malignant phenotypes via activation of PI3K/AKT and MAPK pathways [78–81]. VEGF has an important angiogenic role in ESCC [82].
ADAM17 promotes U87 glioblastoma stem cell migration and invasion
2013, Brain ResearchCitation Excerpt :Stimulation of CD133+ GSCs with the ADAM17 agonist chemokine PMA increased the migrative and invasive abilities of GSCs, while knockdown of ADAM17 expression in GSCs significantly decreased their migration and invasion, indicating that ADAM17 might play a critical role in mediating GSC migration and invasion. Activation of the PI3K/AKT and MEK/ERK pathways, two major pathways coupled to G-protein-coupled chemotactant receptors, is known to be involved in EGFR-mediated tumor invasion (Byun et al., 2009; Dong et al., 2010; Feng et al., 2012; Velpula et al., 2012). EGFR can be activated by its ligands, including TGF-α, TNF-α and amphiregulin, for which ADAM17 is a primary shedding protease (Scheller et al., 2011; Zheng et al., 2012).
Low glucose promotes CD133mAb-elicited cell death via inhibition of autophagy in hepatocarcinoma cells
2013, Cancer LettersCitation Excerpt :New evidence has shown that CD133+ HCC cells contribute to chemoresistance through preferential activation of Akt/PKB and Bcl-2 cell survival response [17]. CD133 overexpression significantly activates Erk [18], endocytosis process and inhibits transferring uptake [19]. Reduction of CD133 in PLC/PRF/5 cells induces a decrease of the mRNA and protein expressions of matrix metalloproteinases [20].
CD133 affects the invasive ability of HCT116 cells by regulating TIMP-2
2013, American Journal of PathologyCitation Excerpt :Tissue specificity may partially account for this difference. CD133 overexpression significantly activated Erk in U87MG human glioblastoma cells,28 and transforming growth factor-β-induced apoptosis in CD133+ cells was blocked by the activation of MEK/ERK signaling in tumorigenic liver stem cells from Mat1a−/− mice.49 No direct relationship between CD133 and MEK/ERK signaling was observed in CRC.
Ovarian cancer stem cell markers: Prognostic and therapeutic implications
2012, Cancer LettersCitation Excerpt :Some studies indicate CD133 functions to promote stem cell self-renewal and suppress differentiation thereby maintaining ‘stemness’. However, this is controversial [70–74]. Preclinical studies demonstrate anti-CD133 antibodies will concentrate in ovarian tumor xenografts suggesting they may be used as imaging agents or therapeutics [75,76].
CD133 <sup>+</sup> liver cancer stem cells modulate radioresistance in human hepatocellular carcinoma
2012, Cancer LettersCitation Excerpt :The activation the MAPK/ERK survival pathway may be involved in the mechanism of radioresistance in these CD133+ liver cancer cells. Recent study by Dong et al. [35] demonstrated that CD133 expression in glioblastoma cells was involved in the activation of MAPK/ERK pathway. This finding was consistent with our result showing that MAPK/ERK was constitutively activated in CD133+ cells postirradiation.