The role of the ShcD and RET interaction in neuroblastoma survival and migration

Mabruk, Zeanap A.; Ahmed, Samrein B M; Thomas, Asha; Prigent, Sally A.

doi:10.1016/j.bbrep.2018.01.007

Cited by 3 publications

(3 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In 2007, ShcD was first identified as a positive regulator to melanoma cell migration as well as it was found to be upregulated in 50% of invasive and metastatic melanomas (3). Since then, few studies experimented the role of ShcD in cell migration (12,35,36).…”

Section: Discussionmentioning

confidence: 99%

Nischarin negatively impacts ShcD-mediated tumor cell migration

Hago,

Wong,

Hachim

et al. 2023

Preprint

View full text Add to dashboard Cite

ShcD was previously found to promote cell motility in melanoma cells. Screening of a yeast two hybrid mouse embryo cDNA library identified Nischarin, a negative regulator to cell motility, as an interacting partner to the ShcD-CH2 domain. Therefore, we aimed to investigate the interaction between Nischarin and ShcD in mammalian cells and to determine their functional impact on cell migration. The Nischarin/ShcD interaction was confirmed by transfection and co-immunoprecipitation assays using full-length constructs in HEK293, MCF7 and MM253 cell lines. Deletion of the first 93 amino acids of ShcD abrogated the interaction indicating the importance of these residues for Nischarin binding. Co-expression of Nischarin and ShcD demonstrated an inhibitory effect on the levels of phospho-ERK and phospho-LIMK. In support of this, Nischarin was found to block the migratory activities of ShcD. A brief in silico analysis of publicly available breast cancer patient data was performed to elucidate the effect of Nischarin/ShcD co-expression on the patients’ overall survival. Patients with high expression of both proteins had better survival than those with only ShcD overexpression. Our results reveal that the novel protein Nischarin is an interacting partner to ShcD. In addition, we report that the tumour suppressive abilities of Nischarin can overcome ShcD-mediated cell migration when both proteins are concomitantly expressed.*This abstract was presented in the National Cancer Research Institute (NCRI)-2019

show abstract

Section: Discussionmentioning

confidence: 99%

Nischarin negatively impacts ShcD-mediated tumor cell migration

Hago,

Wong,

Hachim

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

“…Initially, Iwamoto et al [50] reported neuroblastoma development in a transgenic mouse that carried the RET oncogene driven by a mouse metallothionein regulatory element. Additional reports using cell lines support a role for GDNF/RET signaling in differentiation, migration, and metastasis [51][52][53][54][55][56]. Recently, using neuroblastoma models carrying activating Alk mutations in the context of MYCN overexpression, Cazes et al [57] demonstrated that RET is upregulated in an ALK-dependent fashion.…”

Section: Retmentioning

confidence: 98%

Systematic review of the receptor tyrosine kinase superfamily in neuroblastoma pathophysiology

Rozen

Shohet

2021

Cancer Metastasis Rev

View full text Add to dashboard Cite

Background Neuroblastoma is a devastating disease accounting for 15% of all childhood cancer deaths. Yet, our understanding of key molecular drivers such as receptor tyrosine kinases (RTKs) in this pathology remains poorly clarified. Here, we provide a systematic analysis of the RTK superfamily in the context of neuroblastoma pathogenesis. Methods Statistical correlations for all RTK family members’ expression to neuroblastoma patient survival across 10 independent patient cohorts were annotated, synthesized, and ranked using the R2: Genomics Analysis and Visualization Platform. Gene expression of selected members across different cancer cell lines was further analyzed in the Cancer Cell Line Encyclopedia, part of the Cancer Dependency Map portal (depmap portal (http://depmap.org)). Finally, we provide a detailed literature review for highly ranked candidates. Results Our analysis defined two subsets of RTKs showing robust associations with either better or worse survival, constituting potential novel players in neuroblastoma pathophysiology, diagnosis, and therapy. We review the available literature regarding the oncogenic functions of these RTKs, their roles in neuroblastoma pathophysiology, and potential utility as therapeutic targets. Conclusions Our systematic analysis and review of the RTK superfamily in neuroblastoma pathogenesis provides a new resource to guide the research community towards focused efforts investigating signaling pathways that contribute to neuroblastoma tumor establishment, growth, and/or aggressiveness and targeting these druggable molecules in novel therapeutic strategies.

show abstract

“…Binding of RET to the specific soluble ligand, glial-derived neurotrophic factor (GDNF), is very efficacious in activating pathways that are important for regulating enzymes or those which affect cell proliferation, differentiation, migration, and survival. As a result, overexpression of RET will end in tumor progression and metastasis in NB (Mabruk, Ahmed, Thomas, & Prigent, 2018). This provides a wide spectrum to investigate drugs that are helpful in this situation.…”

Section: Retmentioning

confidence: 99%

Neuroblastoma‐targeted nanoparticles and novel nanotechnology‐based treatment methods

Mobasheri

Rayzan

Shabani

et al. 2020

Journal Cellular Physiology

View full text Add to dashboard Cite

Neuroblastoma is a complicated pediatric tumor, originating from the neural crest, which is the most prevalent in adrenal glands, but may rarely be seen in some other tissues as well. Studies are focused on developing new strategies through novel chemo-and immuno-therapeutic drug targets. Different types of oncogenes such as MYCN, tumor suppressor genes such as p53, and some structural genes such as vascular endothelial growth factor are considered as targets for neuroblastoma therapy. The individual expression patterns in NB cells make them appropriate for this purpose. The combined effect of nano-drug delivery systems and specific drug targets will result in lower systemic side effects, prolonged therapeutic effects, and improvements in the pharmacokinetic properties of the drugs. Some of these novel drug delivery systems with a focus on liposomes as carriers are also discussed. In this review, genes and protein products that are beneficial as drug targets in the treatment of neuroblastoma have been discussed.

show abstract

The role of the ShcD and RET interaction in neuroblastoma survival and migration

Cited by 3 publications

References 35 publications

Nischarin negatively impacts ShcD-mediated tumor cell migration

Nischarin negatively impacts ShcD-mediated tumor cell migration

Systematic review of the receptor tyrosine kinase superfamily in neuroblastoma pathophysiology

Neuroblastoma‐targeted nanoparticles and novel nanotechnology‐based treatment methods

Contact Info

Product

Resources

About