Overexpression of CD133 promotes the phosphorylation of Erk in U87MG human glioblastoma cells

Dong, Lin; Qi, Nan; Rui-min, GE; Cao, Cuili; Lan, Feng; Shen, Li

doi:10.1016/j.neulet.2010.08.057

Cited by 24 publications

(19 citation statements)

References 21 publications

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“…CD133 had been shown to promote TIC or malignant phenotypes by increasing the expression of ABCB5, or activating AKT, IL-8 and MAPK/ERK pathways. 28, 29, 30, 31 It was also reported that CD133 silencing can induce cancer cell cycle arrest by inhibiting expression of cytokinesis-related genes. 32 Whether these or other novel mechanisms are operative in CD133 + ESCC cells remains to be explored.…”

Section: Discussionmentioning

confidence: 97%

MicroRNA-377 suppresses initiation and progression of esophageal cancer by inhibiting CD133 and VEGF

et al. 2017

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Esophageal cancer is one of the most lethal cancers worldwide with poor survival and limited therapeutic options. The discovery of microRNAs created a new milestone in cancer research. miR-377 is located in chromosome region 14q32, which is frequently deleted in esophageal squamous cell carcinoma (ESCC), but the biological functions, clinical significance and therapeutic implication of miR-377 in ESCC are largely unknown. In this study, we found that miR-377 expression was significantly downregulated in tumor tissue and serum of patients with ESCC. Both tumor tissue and serum miR-377 expression levels were positively correlated with patient survival. Higher serum miR-377 expression was inversely associated with pathologic tumor stage, distant metastasis, residual tumor status and chemoradiotherapy resistance. The roles of miR-377 in suppressing tumor initiation and progression, and the underlying molecular mechanisms were investigated. Results of in vitro and in vivo experiments showed that miR-377 overexpression inhibited the initiation, growth and angiogenesis of ESCC tumors as well as metastatic colonization of ESCC cells, whereas silencing of miR-377 had opposite effects. Mechanistically, miR-377 regulated CD133 and VEGF by directly binding to their 3′ untranslated region. Moreover, systemic delivery of formulated miR-377 mimic not only suppressed tumor growth in nude mice but also blocked tumor angiogenesis and metastasis of ESCC cells to the lungs without overt toxicity to mice. Collectively, our study established that miR-377 plays a functional and significant role in suppressing tumor initiation and progression, and may represent a promising non-invasive diagnostic and prognostic biomarker and therapeutic strategy for patients with ESCC.

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Section: Discussionmentioning

confidence: 97%

MicroRNA-377 suppresses initiation and progression of esophageal cancer by inhibiting CD133 and VEGF

et al. 2017

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“…MAPK/ERK activation also participated in the protein kinase C-eta isoform-induced proliferation of glioblastoma cells [21]. Recently, activation of this signaling pathway was reported in CD133 + glioblastoma stem cells, suggesting its possible role in the maintenance of cancer stem cell stemness [22]. New evidences also indicated that PTPIP51 accelerated the formation of human glioblastoma via activating MAPK/ERK pathway [23].…”

Section: Discussionmentioning

confidence: 97%

Oleanolic Acid Suppresses Migration and Invasion of Malignant Glioma Cells by Inactivating MAPK/ERK Signaling Pathway

et al. 2013

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Mitogen-activated protein kinases/Extracellular signal-regulated kinase (MAPK/ERK) pathway is essential for migration and invasion of malignant glioma. It is efficient to inhibit migration and invasion of glioma cells by targeting this pathway. Oleanolic acid (OA) has been well demonstrated to suppress survival, growth and angiogenesis of glioma cells. However, it is still unknown if OA affects the migration and invasion of glioma cells. We utilized U-87 MG glioma cell lines and primary glioma cells from patients to study the effect of OA on migration and invasion of glioma cells with multidisciplinary approaches. In this study, we found that OA significantly decreased the ability of glioma cells to migrate and invade. Epithelial-mesenchymal transition (EMT) of glioma cells was also suppressed by OA treatment. Furthermore, MAPK/ERK pathway was greatly inhibited in glioma cells under OA treatment. MAPK/ERK reactivation induced by a recombinant lentiviral vector, Lv-MEK, was able to rescue the inhibitory effect of OA on migration and invasion of glioma cells. Taken together, we provided evidences that OA was a MAPK/ERK pathway-targeting anti-tumor agent. Although the concentrations we used exceeded its physiological level, OA may be used to prevent migration and invasion of glioma cells by developing its derivatives with enhanced bioactivity.

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“…Glioma cells were transfected with pHBLV-CMVIE-IRES-Puro-CD133 vector according to previously described methods [30], followed by selection in DMEM medium containing puromycin for one week.…”

Section: Methodsmentioning

confidence: 99%

Resistance of glioma cells to nutrient-deprived microenvironment can be enhanced by CD133-mediated autophagy

et al. 2016

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CD133 is a pentaspan transmembrane protein that can serve as a biomarker for cancer stem cells, although its biochemical mechanism remains unclear. Here we report that CD133 expression enhances glioma cell tolerance of a nutrient-deprived microenvironment. Under starvation conditions, CD133-positive cells exhibited higher survival and decreased levels of apoptosis. These changes were dependent on activation of autophagy-associated gene signaling and were impaired by the autophagic inhibitor chloroquine. Furthermore, rapamycin up-regulated the level of autophagy and inversely reduced CD133 expression. Immunofluorescence confirmed that starvation promoted release of CD133 from the plasma membrane to the cytoplasm, with CD133 also partially co-localizing with LC3 upon starvation. Additionally, CD133 partially co-localized with Beclin1, Atg5, and lysosomes, indicating that CD133 directly participates in the autophagosome membrane fusion process and ultimately undergoes lysosomal degradation. Collectively, our results demonstrate that CD133 contributes to cell survival by regulating autophagy, and that targeting CD133-linked signaling and autophagy may be useful in improving anti-cancer treatments.

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Overexpression of CD133 promotes the phosphorylation of Erk in U87MG human glioblastoma cells

Cited by 24 publications

References 21 publications

MicroRNA-377 suppresses initiation and progression of esophageal cancer by inhibiting CD133 and VEGF

MicroRNA-377 suppresses initiation and progression of esophageal cancer by inhibiting CD133 and VEGF

Oleanolic Acid Suppresses Migration and Invasion of Malignant Glioma Cells by Inactivating MAPK/ERK Signaling Pathway

Resistance of glioma cells to nutrient-deprived microenvironment can be enhanced by CD133-mediated autophagy

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