ArticleInternational journal of molecular sciences2023
Low-Density Lipoprotein Receptor Is a Key Driver of Aggressiveness in Thyroid Tumor Cells.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Partial Remission Without Recurrence in a 9-Year-Old Golden Retriever with Nasal Carcinoma Treated with Prednisolone/Chlorambucil Metronomic Combination Therapy: A Case Report and Literature Review of Molecular Mechanisms.Current issues in molecular biology · 2025Article
- Single-cell perspective on the Monocyte-to-HDL cholesterol ratio as a metastasis biomarker in papillary thyroid cancer.BMC cancer · 2025Article
- Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- HPV-Associated Gene Signatures in Bladder Cancer: A Comprehensive Prognostic Model and its Implications in Immunotherapy.International journal of medical sciences · 2025Article
- Comprehensive Mendelian randomization analysis of low-density lipoprotein cholesterol and multiple cancers.Discover oncology · 2024Article
- Apolipoproteins in Health and Disease.International journal of molecular sciences · 2024Article
- Development and validation of prediction models for papillary thyroid cancer structural recurrence using machine learning approaches.BMC cancer · 2024Article
- Inhibition of PCSK9: A Promising Enhancer for Anti-PD-1/PD-L1 Immunotherapy.Research (Washington, D.C.) · 2024Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously described the role of low-density lipoprotein (LDL) in aggressiveness in papillary thyroid cancer (PTC). Moreover, the MAPK signaling pathway in the presence of BRAF V600E mutation is associated with more aggressive PTC. Although the link between MAPK cascade and LDL receptor (LDLR) expression has been previously described, it is unknown whether LDL can potentiate the adverse effects of PTC through it. We aimed to investigate whether the presence of LDL might accelerate the oncogenic processes through MAPK pathway in presence or absence of BRAF V600E in two thyroid cell lines: TPC1 and BCPAP (wild-type and BRAF V600E, respectively). LDLR, PI3K-AKT and RAS/RAF/MAPK (MEK)/ERK were analyzed via Western blot; cell proliferation was measured via MTT assay, cell migration was studied through wound-healing assay and LDL uptake was analyzed by fluorometric and confocal analysis. TPC1 demonstrated a time-specific downregulation of the LDLR, while BCPAP resulted in a receptor deregulation after LDL exposition. LDL uptake was increased in BCPAP over-time, as well as cell proliferation (20% higher) in comparison to TPC1. Both cell lines differed in migration pattern with a wound closure of 83.5 ± 9.7% after LDL coculture in TPC1, while a loss in the adhesion capacity was detected in BCPAP. The siRNA knockdown of LDLR in LDL-treated BCPAP cells resulted in a p-ERK expression downregulation and cell proliferation modulation, demonstrating a link between LDLR and MAPK pathway. The modulation of BRAF-V600E using vemurafenib-impaired LDLR expression decreased cellular proliferation. Our results suggest that LDLR regulation is cell line-specific, regulating the RAS/RAF/MAPK (MEK)/ERK pathway in the LDL-signaling cascade and where BRAF V600E can play a critical role. In conclusion, targeting LDLR and this downstream signaling cascade, could be a new therapeutic strategy for PTC with more aggressive behavior, especially in those harboring BRAF V600E.
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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 Socratic graph.