Data on the number and frequency of scientific literature citations for established medulloblastoma cell lines

Ivanov, Delyan P.; Walker, David; Coyle, Beth; Grabowska, Anna

doi:10.1016/j.dib.2016.10.004

Cited by 7 publications

(9 citation statements)

References 4 publications

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“…2A). These D283-Med cells were defined as having loss of copy number variations within the genomic region of the PRUNE1, OTX2, c-MYC, N-MYC and TP53 genes, and lower expression of the NME1 and NME2 genes compared to the other MB group3 cell lines for TP53 status (Ivanov et al, 2016).…”

Section: Prune1 and Otx2 Expression Correlate With Canonical Tgf-b Simentioning

confidence: 99%

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Metastatic group 3 medulloblastoma is driven by PRUNE1 targeting NME1–TGF-β–OTX2–SNAIL via PTEN inhibition

Ferrucci

Antonellis

Pennino

et al. 2018

Brain

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Genetic modifications during development of paediatric groups 3 and 4 medulloblastoma are responsible for their highly metastatic properties and poor patient survival rates. PRUNE1 is highly expressed in metastatic medulloblastoma group 3, which is characterized by TGF-β signalling activation, c-MYC amplification, and OTX2 expression. We describe the process of activation of the PRUNE1 signalling pathway that includes its binding to NME1, TGF-β activation, OTX2 upregulation, SNAIL (SNAI1) upregulation, and PTEN inhibition. The newly identified small molecule pyrimido-pyrimidine derivative AA7.1 enhances PRUNE1 degradation, inhibits this activation network, and augments PTEN expression. Both AA7.1 and a competitive permeable peptide that impairs PRUNE1/NME1 complex formation, impair tumour growth and metastatic dissemination in orthotopic xenograft models with a metastatic medulloblastoma group 3 cell line (D425-Med cells). Using whole exome sequencing technology in metastatic medulloblastoma primary tumour cells, we also define 23 common 'non-synonymous homozygous' deleterious gene variants as part of the protein molecular network of relevance for metastatic processes. This PRUNE1/TGF-β/OTX2/PTEN axis, together with the medulloblastoma-driver mutations, is of relevance for future rational and targeted therapies for metastatic medulloblastoma group 3.10.1093/brain/awy039_video1awy039media15742053534001.

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Section: Prune1 and Otx2 Expression Correlate With Canonical Tgf-b Simentioning

confidence: 99%

“…Mutational status is indicated by the dots. Sources for data: published TP53 status for all samples (Ivanov et al, 2016); complete NGS-WES data available for MB Group3 D341-Med and MB SHH DAOY (http://www.cbioportal. org), MB Group3 D283-Med (http://cancer.sanger.ac.uk/cosmic).…”

Section: Prune1 Sustains Oncogenic Pathways In Medulloblastoma Througmentioning

confidence: 99%

Metastatic group 3 medulloblastoma is driven by PRUNE1 targeting NME1–TGF-β–OTX2–SNAIL via PTEN inhibition

Ferrucci

Antonellis

Pennino

et al. 2018

Brain

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“…GRK2 binds to PTCH1 through the GRK2 PTCH1-binding region to block PTCH1 binding to cyclin B1, thus relieving the inhibition on nuclear accumulation of cyclin B1 and promoting cell cycle progression 68 . We found a medulloblastoma-promoting effect of GRK2 in two SHH subgroup medulloblastoma cell lines, UW228 and Daoy 95–97 . The small number of SHH subgroup medulloblastoma cell lines that are available 95–97 was limiting in terms of testing additional lines.…”

Section: Discussionmentioning

confidence: 73%

“…We found a medulloblastoma-promoting effect of GRK2 in two SHH subgroup medulloblastoma cell lines, UW228 and Daoy 95–97 . The small number of SHH subgroup medulloblastoma cell lines that are available 95–97 was limiting in terms of testing additional lines. Additionally, our experiments were unable to determine if the growth-promoting and protective roles of GRK2 were related to SHH pathway activation or independent of it.…”

Section: Discussionmentioning

confidence: 73%

GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis

Pathania

Ren

Mahdi

et al. 2019

Sci Rep

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G-protein coupled receptor kinase 2 (GRK2; ADRBK1, BARK1) is most known as a regulator of G-protein coupled receptors. However, GRK2 also has other functions. Medulloblastomas are the most common malignant brain cancers in children. GRK2 has not been implicated in medulloblastoma biology. Here we report that GRK2 knockdown slowed cell growth, diminished proliferation, and enhanced cisplatin- and etoposide-induced apoptosis in medulloblastoma cell lines UW228-2 and Daoy. Reciprocally, GRK2 overexpression attenuated apoptosis induced by these chemotherapy drugs. Cisplatin and etoposide increased phosphorylation of AKT (S473) and GRK2 knockdown mitigated this increase. Cisplatin and etoposide attenuated ERK phosphorylation, but GRK2 knockdown did not alter this effect. Wildtype GRK2 reversed the increase in cisplatin- and etoposide-induced apoptosis caused by GRK2 knockdown. GRK2-K220R (kinase dead) and GRK2-S670A (unphosphorylated, constitutively active) conferred protection from cisplatin that was similar to wildtype GRK2, suggesting that this protection may be mediated though a kinase-independent activity of GRK2. These data demonstrate that GRK2 contributes to proliferation and survival of these medulloblastoma cell lines and to their protection from cisplatin- and etoposide-induced apoptosis.

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“…Similar works can be considered, see [4] , [5] , [6] , [7] , [8] , [9] , [10] , [11] , [12] , [13] , [14] , [15] , [16] , [17] , [18] , [19] , [20] , [21] , [22] , [23] , [24] , [25] .…”

Section: Experimental Design Materials and Methodsunclassified

Analysis of dataset on editorial board composition of Dove Medical Press by continent

et al. 2018

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This article presents the frequency of distribution of editorial members of Dove Medical press, across the world based on their official stated affiliations. Uneven distributions across the six continents were observed and this was confirmed by the Chi-square test of goodness of fit. Further research can focus on data on the gender composition, distribution of the affiliations of the first or corresponding authors of the respective journals, citation and editorial board composition based on the abstraction and indexation of the journals.

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Data on the number and frequency of scientific literature citations for established medulloblastoma cell lines

Cited by 7 publications

References 4 publications

Metastatic group 3 medulloblastoma is driven by PRUNE1 targeting NME1–TGF-β–OTX2–SNAIL via PTEN inhibition

Metastatic group 3 medulloblastoma is driven by PRUNE1 targeting NME1–TGF-β–OTX2–SNAIL via PTEN inhibition

GRK2 promotes growth of medulloblastoma cells and protects them from chemotherapy-induced apoptosis

Analysis of dataset on editorial board composition of Dove Medical Press by continent

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