ArticleInternational journal of oncology2018
LRIG1 negatively regulates RET mutants and is downregulated in thyroid cancer.
Article in International journal of oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Hsa-miR-21 promoted the progression of lung adenocarcinoma by regulating LRIG1 expression.BMC pulmonary medicine · 2025Article
- Prognostic model construction and immune microenvironment analysis of esophageal cancer based on gene expression data and microRNA target genes.Translational cancer research · 2023Article
- Aberrant promoter methylation contributes to LRIG1 silencing in basal/triple-negative breast cancer.British journal of cancer · 2022Article
- Lobectomy may be more appropriate for patients with early-stage medullary thyroid cancer older than 60 years old.Frontiers in endocrinology · 2022Article
- Epigenetic loss of heterozygosity of Apc and an inflammation-associated mutational signature detected in Lrig1BMC cancer · 2020Article
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Authors and funding
11 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Papillary thyroid carcinoma (PTC) and medullary thyroid carcinoma (MTC) are characterized by genomic rearrangements and point mutations in the proto-oncogene RET. Leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1) is a suppressor of various receptor tyrosine kinases, including RET. LRIG1 expression levels are associated with patient survival in many cancer types. In the present study, we investigated whether the oncogenic RET mutants RET2A (C634R) and RET2B (M918T) were regulated by LRIG1, and the possible effects of LRIG1 expression in thyroid cancer were investigated in three different clinical cohorts and in a RET2B-driven mouse model of MTC. LRIG1 was shown to physically interact with both RET2A and RET2B and to restrict their ligand-independent activation. LRIG1 mRNA levels were downregulated in PTC and MTC compared to normal thyroid gland tissue. There was no apparent association between LRIG1 RNA or protein expression levels and patient survival in the studied cohorts. The transgenic RET2B mice developed pre-cancerous medullary thyroid lesions at a high frequency (36%); however, no overt cancers were observed. There was no significant difference in the incidence of pre-cancerous lesions between Lrig1 wild-type and Lrig1-deficient RET2B mice. In conclusion, the findings that LRIG1 is a negative regulator of RET2A and RET2B and is also downregulated in PTC and MTC may suggest that LRIG1 functions as a thyroid tumor suppressor.
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