ArticleCancer science2013
Novel adaptor protein Shf interacts with ALK receptor and negatively regulates its downstream signals in neuroblastoma.
Article in Cancer science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Plasma Exosome Gene Signature Differentiates Colon Cancer from Healthy Controls.Annals of surgical oncology · 2023Article
- SHF Acts as a Novel Tumor Suppressor in Glioblastoma Multiforme by Disrupting STAT3 Dimerization.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Integrated analysis of human genetic association study and mouse transcriptome suggests LBH and SHF genes as novel susceptible genes for amyloid-β accumulation in Alzheimer's disease.Human genetics · 2018Article
- BMCC1, which is an interacting partner of BCL2, attenuates AKT activity, accompanied by apoptosis.Cell death & disease · 2015Article
- Unravelling the RNA-Binding Properties of SAFB Proteins in Breast Cancer Cells.BioMed research international · 2015Article
- ALK gene amplification is associated with poor prognosis in colorectal carcinoma.British journal of cancer · 2013Article
- Novel adaptor protein Shf interacts with ALK receptor and negatively regulates its downstream signals in neuroblastoma.Cancer science · 2013Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our neuroblastoma cDNA project previously identified Src homology 2 domain containing F (Shf) as one of the genes expressed at high levels in favorable neuroblastoma. Shf is an adaptor protein containing four putative tyrosine phosphorylation sites and an SH2 domain. In this study, we found that Shf interacted with anaplastic lymphoma kinase (ALK), an oncogenic receptor tyrosine kinase in neuroblastoma. Real-time PCR analysis showed that Shf mRNA is highly expressed in non-metastatic neuroblastomas compared to metastatic tumor samples (P < 0.030, n = 106). Interestingly, patients showing high ALK and low Shf mRNA expressions showed poor prognosis, whereas low ALK and high Shf expressions were related to better prognosis (P < 0.023, n = 38). Overexpression of ALK and siRNA-mediated knockdown of Shf yielded similar results, such as an increase in cellular growth and phosphorylation of ALK, in addition to Erk1/2 and signal transducer and activator of transcription 3 (STAT3) that are downstream signals of the ALK-initiated phospho-transduction pathway. Knockdown of Shf also increased the cellular mobility and invasive capability of neuroblastoma cells. These results suggest that Shf interacts with ALK and negatively regulates the ALK-initiated signal transduction pathway in neuroblastoma. We thus propose that Shf inhibits phospho-transduction signals mediated by ALK, which is one of the major key players on neuroblastoma development, resulting in better prognosis of the tumor.
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