ArticleOncogene2004
Functional expression of the CXCR4 chemokine receptor is induced by RET/PTC oncogenes and is a common event in human papillary thyroid carcinomas.
Article in Oncogene, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.
- Causal relationship between inflammatory cytokines and autoimmune thyroid disease: a bidirectional two-sample Mendelian randomization analysis.Frontiers in immunology · 2024Pooled it
- PRECISE: A Prognostic Thyrocyte-Derived Gene Signature for Papillary Thyroid Carcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2026Article
- Molecular genetics, therapeutics and RET inhibitor resistance for medullary thyroid carcinoma and future perspectives.Cell communication and signaling : CCS · 2024Review
- Article
- Coexisting CLT in PTC is an independent predictor of tumor aggressiveness for patients aged under 55: a retrospective analysis of 635 patients.BMC endocrine disorders · 2022Article
- The Genomic Landscape of Thyroid Cancer Tumourigenesis and Implications for Immunotherapy.Cells · 2021Review
- Immune and Inflammatory Cells in Thyroid Cancer Microenvironment.International journal of molecular sciences · 2019Review
- AXL Is a Novel Predictive Factor and Therapeutic Target for Radioactive Iodine Refractory Thyroid Cancer.Cancers · 2019Article
- Article
- BRAF V600E and RET/PTC Promote the Activity of Nuclear Factor-κB, Inflammatory Mediators, and Lymph Node Metastasis in Papillary Thyroid Carcinoma: A Study of 50 Patients in Inner Mongolia.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- CXCR4 Based Therapeutics for Non-Small Cell Lung Cancer (NSCLC).Journal of clinical medicine · 2018Review
- Quercetin inhibits NTHi-triggered CXCR4 activation through suppressing IKKα/NF-κB and MAPK signaling pathways in otitis media.International journal of molecular medicine · 2018Article
- Article
- GDNF and the RET Receptor in Cancer: New Insights and Therapeutic Potential.Frontiers in physiology · 2018Review
- Pharmacological targeting of CXCL12/CXCR4 signaling in prostate cancer bone metastasis.Molecular cancer · 2016Article
- Effect of CXCL12/CXCR4 on increasing the metastatic potential of non-small cell lung cancerOncology letters · 2014Article
- Deregulation of microRNA expression in thyroid tumors.Journal of Zhejiang University. Science. B · 2014Review
- Deregulation of microRNA expression in thyroid neoplasias.Nature reviews. Endocrinology · 2014Review
- CXC chemokine receptor 4 expression, CXC chemokine receptor 4 activation, and wild-type nucleophosmin are independently associated with unfavorable prognosis in patients with acute myeloid leukemia.Clinical lymphoma, myeloma & leukemia · 2013Article
- Different CXCR4 expression according to various histologic subtype of papillary thyroid carcinoma.Endocrine pathology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To identify genes involved in the transformation of thyroid follicular cells, we explored, using DNA oligonucleotide microarrays, the transcriptional response of PC Cl3 rat thyroid epithelial cells to the ectopic expression of the RET/PTC oncogenes. We found that RET/PTC was able to induce the expression of CXCR4, the receptor for the chemokine CXCL12/SDF-1alpha/beta. We observed that CXCR4 expression correlated with the transforming ability of the oncoprotein and depended on the integrity of the RET/PTC-RAS/ERK signaling pathway. We found that CXCR4 was expressed in RET/PTC-positive human thyroid cancer cell lines, but not in normal thyroid cells. Furthermore, we found CXCR4 expression in human thyroid carcinomas, but not in normal thyroid samples by immunohistochemistry. Since CXCR4 has been recently implicated in tumor proliferation, motility and invasiveness, we asked whether treatment with SDF-1alpha was able to induce a biological response in thyroid cells. We observed that SDF-1alpha induced S-phase entry and survival of thyroid cells. Invasion through a reconstituted extracellular matrix was also supported by SDF-1alpha and inhibited by a blocking antibody to CXCR4. Taken together, these results suggest that human thyroid cancers bearing RET/PTC rearrangements may use the CXCR4/SDF-1alpha receptor-ligand pathway to proliferate, survive and migrate.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.