Proliferation and Survival of Embryonic Sympathetic Neuroblasts by MYCN and Activated ALK Signaling

Krämer, Marco; Ribeiro, Diogo; Arsenian-Henriksson, Marie; Deller, Thomas; Rohrer, Hermann

doi:10.1523/jneurosci.0183-16.2016

Cited by 42 publications

(48 citation statements)

References 78 publications

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“…The activation of adaptor proteins and other cellular proteins, such as protein tyrosine phosphatase, non‐receptor type 11, SRC, fibroblast growth factor receptor substrate 2, and SHC, has been observed downstream of ALK, implicating roles for these alternative pathways . Other reported ALK downstream targets are Bcl‐2‐like protein 11, p27, Cyclin D2, nuclear interacting partner of ALK, Ras‐related C3 botulinum toxin substrate 1, cell division cycle 42, p130CAS, Src homology region 2 domain‐containing phosphatase‐1, and PIKFYVE …”

Section: Structure Function and Alk Signalingmentioning

confidence: 99%

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The role of anaplastic lymphoma kinase in pediatric cancers

Takita

2017

Cancer Science

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The anaplastic lymphoma kinase (ALK) gene was initially identified as a fusion partner of the nucleophosmin gene in anaplastic large‐cell lymphoma with t(2;5)(p23;q35) translocation, and then described with different genetic abnormalities in a number of tumors. Although ALK is known to be involved in the pathogenesis of neuroblastoma through activating mutations or gene amplification, its role in the pathogenesis of other pediatric cancers is still elusive. In addition to neuroblastoma, the high‐grade amplification of ALK has been described in a subset of rhabdomyosarcoma cases. Normal ALK protein expression is restricted to the nervous systems of adult mammals, but the aberrant expression of ALK has been observed in a variety of pediatric cancers, including glioma and Ewing sarcoma. The discovery of oncogenic activation of ALK in neuroblastoma suggests that this cancer could be potentially treated with an ALK inhibitor, as could other cancers, such as non‐small‐cell lung cancer and anaplastic large‐cell lymphoma. However, cellular responses to mutant ALK are complex when compared to rearranged ALK, and treatment remains a challenge. This review focuses on the biology of ALK in pediatric cancers and possible therapeutic strategies for ALK‐associated tumors.

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Section: Structure Function and Alk Signalingmentioning

confidence: 99%

“…(17) Other reported ALK downstream targets are Bcl-2-like protein 11, p27, Cyclin D2, nuclear interacting partner of ALK, Ras-related C3 botulinum toxin substrate 1, cell division cycle 42, p130CAS, Src homology region 2 domain-containing phosphatase-1, and PIKFYVE. (23)(24)(25)(26)…”

Section: Structure Function and Alk Signalingmentioning

confidence: 99%

The role of anaplastic lymphoma kinase in pediatric cancers

Takita

2017

Cancer Science

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“…terminal differentiation and functionality of sympathetic neurons (22)(23)(24), although this remains controversial (9,(25)(26)(27). Postnatally, MycN is not expressed in the sympathetic ganglia (16).…”

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confidence: 99%

Enhanced expression of MycN/CIP2A drives neural crest toward a neural stem cell-like fate: Implications for priming of neuroblastoma

Kerosuo

Neppala

Hsin

et al. 2018

Proc. Natl. Acad. Sci. U.S.A.

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Neuroblastoma is a neural crest-derived childhood tumor of the peripheral nervous system in which MycN amplification is a hallmark of poor prognosis. Here we show that is expressed together with phosphorylation-stabilizing factor in regions of the neural plate destined to form the CNS, but MycN is excluded from the neighboring neural crest stem cell domain. Interestingly, ectopic expression of MycN or CIP2A in the neural crest domain biases cells toward CNS-like neural stem cells that express Sox2. Consistent with this, some forms of neuroblastoma have been shown to share transcriptional resemblance with CNS neural stem cells. As high levels correlate with poor prognosis, we posit that a MycN/CIP2A-mediated cell-fate bias may reflect a possible mechanism underlying early priming of some aggressive forms of neuroblastoma. In contrast to, its paralogue is normally expressed in the neural crest stem cell domain and typically is associated with better overall survival in clinical neuroblastoma, perhaps reflecting a more "normal" neural crest-like state. These data suggest that priming for some forms of aggressive neuroblastoma may occur before neural crest emigration from the CNS and well before sympathoadrenal specification.

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“…The inhibition of RICTOR, which is part of the mTOR pathway, reveals the MP radiation impact on cell growth and survival and on oxidative phosphorylation and other mitochondrial functions (Li, Long, He, Belshaw, & Scott, 2015). The activation of NKX2-3 and MYCN, which are implicated in cell differentiation and oncogenesis (Kramer, Ribeiro, Arsenian-Henriksson, Deller, & Rohrer, 2016;Nagel et al, 2017), could be associated with previously reported brain protein expression alterations related to neurogenesis and brain plasticity demonstrated by Salford's group (Nittby, Grafstrom, et al, 2008) and our group , as well as with increased risk for brain tumor development (Hardell & Carlberg, 2009) following exposure to MP radiation. Finally, the activation of the last two regulators (IL-10 and EPO), which are cytokines related to microglia and implicated in inflammatory processes, neurodegenerative disorders, brain injuries, and antiapoptotic functions (Lobo-Silva, Carriche, , Roque, & Saraiva, 2016;Tamura et al, 2017), may be related to the robust EPA decrease that we found and to the cognitive dysfunction previously reported by our group following MP radiation exposure (Fragopoulou et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

et al. 2018

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BackgroundThe widespread use of wireless devices during the last decades is raising concerns about adverse health effects of the radiofrequency electromagnetic radiation (RF‐EMR) emitted from these devices. Recent research is focusing on unraveling the underlying mechanisms of RF‐EMR and potential cellular targets. The “omics” high‐throughput approaches are powerful tools to investigate the global effects of RF‐EMR on cellular physiology.MethodsIn this work, C57BL/6 adult male mice were whole‐body exposed (nE xp = 8) for 2 hr to GSM 1800 MHz mobile phone radiation at an average electric field intensity range of 4.3–17.5 V/m or sham‐exposed (nSE = 8), and the RF‐EMR effects on the hippocampal lipidome and transcriptome profiles were assessed 6 hr later.ResultsThe data analysis of the phospholipid fatty acid residues revealed that the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega‐3 (EPA, 20:5 ω3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group. The observed changes indicate a membrane remodeling response of the tissue phospholipids after nonionizing radiation exposure, reducing SFA and EPA, while increasing MUFA residues. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p < 0.05) between the two groups, revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis.ConclusionsThis study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits previously shown by our group.

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Proliferation and Survival of Embryonic Sympathetic Neuroblasts by MYCN and Activated ALK Signaling

Cited by 42 publications

References 78 publications

The role of anaplastic lymphoma kinase in pediatric cancers

The role of anaplastic lymphoma kinase in pediatric cancers

Enhanced expression of MycN/CIP2A drives neural crest toward a neural stem cell-like fate: Implications for priming of neuroblastoma

Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study

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