ArticleJournal of neuro-oncology2012
Mechanism for the induction of cell death in ONS-76 medulloblastoma cells by Zhangfei/CREB-ZF.
Article in Journal of neuro-oncology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 33 citations in OpenAlex.
- The pivotal role of autophagy in the pathogenesis and therapy of medulloblastoma.Future oncology (London, England) · 2024Review
- CREBZF mRNA nanoparticles suppress breast cancer progression through a positive feedback loop boosted by circPAPD4.Journal of experimental & clinical cancer research : CR · 2023Article
- Neurotrophin Signaling in Medulloblastoma.Cancers · 2020Review
- Interaction between p53 and Ras signaling controls cisplatin resistance via HDAC4- and HIF-1α-mediated regulation of apoptosis and autophagy.Theranostics · 2019Article
- Activation of CREBZF Increases Cell Apoptosis in Mouse Ovarian Granulosa Cells by Regulating the ERK1/2 and mTOR Signaling Pathways.International journal of molecular sciences · 2018Article
- FRK inhibits breast cancer cell migration and invasion by suppressing epithelial-mesenchymal transition.Oncotarget · 2017Article
- Transcriptome analysis reveals long intergenic non-coding RNAs involved in skeletal muscle growth and development in pig.Scientific reports · 2017Article
- Lack of inflammatory gene expression in bats: a unique role for a transcription repressor.Scientific reports · 2017Article
- Mutations in TrkA Causing Congenital Insensitivity to Pain with Anhidrosis (CIPA) Induce Misfolding, Aggregation, and Mutation-dependent Neurodegeneration by Dysfunction of the Autophagic Flux.The Journal of biological chemistry · 2016Article
- Effects of cyclic AMP response element binding protein-Zhangfei (CREBZF) on the unfolded protein response and cell growth are exerted through the tumor suppressor p53.Cell cycle (Georgetown, Tex.) · 2014Article
- CREBZF expression and hormonal regulation in the mouse uterus.Reproductive biology and endocrinology : RB&E · 2013Article
- Kinotypes: stable species- and individual-specific profiles of cellular kinase activity.BMC genomics · 2013Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cells from medulloblastoma lines do not contain detectable amounts of the basic leucine-zipper protein Zhangfei. However, we have previously shown that expression of this protein in cells of the ONS-76 and UW228 medulloblastoma lines causes the cells to stop growing and develop processes that resemble neurites. Our objective was to determine the molecular mechanisms by which Zhangfei influences ONS-76 cells. We infected ONS-76 cells with adenovirus vectors expressing either Zhangfei or the control protein LacZ and then compared the following parameters in Zhangfei and LacZ-expressing cells: (a) markers of apoptosis, autophagy and macropinocytosis, (b) transcripts for genes involved in neurogenesis and apoptosis, (c) phosphorylation of peptide targets of selected cellular protein kinases, and (d) activation of transcription factors. Zhangfei-expressing cells appeared to succumb to apoptosis. Increased staining for autophagic vesicles and upregulated expression of autophagy response genes in these cells indicated that they were undergoing autophagy, possibly associated with apoptosis. Within our analysis, patterns of gene expression and phosphorylation-mediated signal transduction activity in Zhangfei-expressing cells indicated that the mitogen-activated protein kinase (MAPK) pathway was active. In addition, we found that the transcription factor Brn3a as well as factors implicated in differentiation were also active in Zhangfei-expressing cells. We tested the hypothesis that Zhangfei enhances the expression of Brn3a, a known inducer of TrkA, the high-affinity receptor for nerve growth factor (NGF). TrkA then engages NGF in an autocrine manner triggering the MAPK pathway and leading to differentiation of ONS-76 cells into neuron and glia-like cells-a process that eventually brings about cell death. We showed that: (a) Zhangfei could enhance transcription from the isolated Brn3a promoter, (b) ONS-76 cells produced NGF and (c) antibodies against NGF and inhibitors of TrkA and selected components of the MAPK pathway could partially restore the growth of Zhangfei-expressing ONS-76 cells.
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