Low-Density Lipoprotein Receptor Is a Key Driver of Aggressiveness in Thyroid Tumor Cells

Author:

Revilla Giovanna12ORCID,Ruiz-Auladell Lara1,Vallverdú Núria Fucui1,Santamaría Paula13,Moral Antonio45,Pérez José Ignacio4,Li Changda12ORCID,Fuste Victoria6,Lerma Enrique6,Corcoy Rosa1357ORCID,Pitoia Fabián8,Escolà-Gil Joan Carles129ORCID,Mato Eugènia17

Affiliation:

1. Institut de Recerca de l’Hospital de la Santa Creu i Sant Pau, Institut d’Investigació Biomèdica (IIB) Sant Pau, 08041 Barcelona, Spain

2. Department of Biochemistry and Molecular Biology, Universitat Autònoma de Barcelona (UAB), 08025 Barcelona, Spain

3. Department of Endocrinology and Nutrition, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain

4. Department of General Surgery, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain

5. Department of Medicine, Universitat Autònoma de Barcelona (UAB), 08193 Bellaterra, Spain

6. Department of Pathological Anatomy, Hospital de la Santa Creu i Sant Pau, 08041 Barcelona, Spain

7. CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN), 28029 Madrid, Spain

8. Division of Endocrinology, Hospital de Clínicas, University of Buenos Aires, Buenos Aires C1120 AAF, Argentina

9. CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), 28029 Madrid, Spain

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.

Funder

Instituto de Salud Carlos III

Fondo Social Europeo

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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