ArticleOncogene2012
The insulin resistance Grb14 adaptor protein promotes thyroid cancer ret signaling and progression.
Article in Oncogene, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
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- High expression of GRB14 is associated with cancer progression and poor prognosis in gastric cancer.Discover oncology · 2025Article
- GRB14: A prognostic biomarker driving tumor progression in gastric cancer through the PI3K/AKT signaling pathway by interacting with COBLL1.Open life sciences · 2025Article
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- GRB10 is a novel oncogene associated with cell proliferation and prognosis in glioma.Cancer cell international · 2022Article
- Identification of low-dose radiation-induced exosomal circ-METRN and miR-4709-3p/GRB14/PDGFRα pathway as a key regulatory mechanism in Glioblastoma progression and radioresistance: Functional validation and clinical theranostic significance.International journal of biological sciences · 2021Article
- Oncogenic Network and Hub Genes for Natural Killer/T-Cell Lymphoma Utilizing WGCNA.Frontiers in oncology · 2020Article
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- The role of small adaptor proteins in the control of oncogenic signalingr driven by tyrosine kinases in human cancer.Oncotarget · 2016Review
- Selective repression of RET proto-oncogene in medullary thyroid carcinoma by a natural alkaloid berberine.BMC cancer · 2015Article
- An epigenetic map of age-associated autosomal loci in northern European families at high risk for the metabolic syndrome.Clinical epigenetics · 2015Article
- XB130 mediates cancer cell proliferation and survival through multiple signaling events downstream of Akt.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
The growth factor receptor-bound protein (Grb) 14 is an adaptor molecule of the Grb7/10/14 family with characteristic Between Plekstrin and SH2 (BPS) domains serving to avidly bind tyrosine kinases. Grb14 inhibits insulin receptor (IR) catalytic activity through interaction with the BPS domain and impedes peptide substrate binding. Members of this Grb family have also been shown to interact with other kinases through their SH2 domain. Here we examined the functional role of Grb14 in thyroid cancer using loss- and gain-of-function approaches. Stable knockdown of Grb14 in thyroid cancer cells facilitated IR signaling. In contrast, RET phosphorylation was diminished in concert with reduced activation of Akt and signal transducer and activator of transcription 3 (STAT3). Loss of Grb14 also resulted in diminished cell proliferation and invasion both in vitro and in mouse flank xenografts. In complementary studies, forced expression of Grb14 interrupted IR signaling but facilitated RET activation, STAT3 and Akt phosphorylation. Consistent with these findings Grb14 overexpression enhanced cell invasion and resulted in striking metastases in an orthotopic thyroid cancer mouse xenograft model. Primary human thyroid cancer microarrays revealed a positive correlation between Grb14 expression and invasive behavior. Our findings uncover a new role for Grb14 in finely tuning receptor signaling and modulating thyroid cancer progression.
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