ArticleOncology letters2023
Proteomic analysis of radioiodine-refractory differentiated thyroid cancer identifies CHI3L1 upregulation in association with dysfunction of the sodium-iodine symporter.
Article in Oncology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 3 citations in OpenAlex.
- Optimal surgical population for cervical lymph node dissection in PTC.Frontiers in oncology · 2024Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Radioiodine refractory differentiated thyroid cancer (RR-DTC) is the main factor adversely affecting the overall survival rate of patients with thyroid cancer. The aim of the present study was to investigate the underlying molecular mechanism of pathogenesis of RR-DTC and to explore novel therapeutic targets for clinical treatment. A proteomic analysis was performed using the tumor tissues of patients with RR-DTC. A total of 6 metastatic lymph nodes were collected during lymph node dissection, 3 from patients with RR-DTC and 3 from patients with papillary thyroid cancer. The expression of chitinase-3-like 1 (CHI3L1) and sodium-iodine symporter (NIS) in the tumor tissue was detected by immunohistochemistry (IHC). Western blotting was used to detect the expression of CHI3L1, phosphorylated (p)-MEK and p-ERK1/2 in PTC-K1 cells transfected with CHI3L1 overexpression vector. The proteomic analysis identified 665 differentially expressed proteins (DEPs), including 327 upregulated and 338 downregulated proteins in the RR-DTC group, which were enriched in 59 signaling pathways by Kyoto Encyclopedia of Genes and Genomes database analysis. In particular, CHI3L1 was demonstrated to be significantly upregulated in RR-DTC as evidenced by quantitative proteomic analysis and IHC. Western blotting suggested that the overexpression of CHI3L1 activated the MEK/ERK1/2 signaling pathway, which may lead to NIS dysfunction. In conclusion, the present study suggests that CHI3L1 is a potential molecular target for the radiotherapy of patients with RR-DTC.
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