Thyroid cancer cell lines: an overview

Saiselet, Manuel; Floor, Sebastien; Tarabichi, Maxime; Dom, Geert; Hebrant, Aline; Staveren, Wilma C.G. van; Maenhaut, Carine

doi:10.3389/fendo.2012.00133

Cited by 129 publications

(122 citation statements)

References 34 publications

(62 reference statements)

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“…In particular, studies of the thyrocyte and thyroid cancer proteomics, both ex vivo [26][27][28][29] and of cell lines [25] are in a minority compared with studies of the genome and transcriptome [30,31].…”

Section: Discussionmentioning

confidence: 99%

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

Musso

Cara

Albanese

et al. 2013

Journal of Proteomics

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Thyroid carcinomas account for a minority of all malignant tumours but, after those of the gonads, they represent the most common forms of endocrine cancers. They include several types, among which the papillary thyroid cancer (PTC) and the anaplastic thyroid cancer (ATC) are the best known. The two hystotypes display significant biological and clinical differences: PTC is a well differentiated form of tumour with a high incidence and a good prognosis, while the ATC is less frequent but represents one of the most aggressive endocrine tumours with morphological features of an undifferentiated type. To date, as far as we know, no conclusive studies, useful to design arrays of molecular markers, have been published illustrating the phenotypic and proteomic differences between these two tumours. The aim of this work was to perform a comparative analysis of two thyroid cancer cell lines, derived respectively from papillary (BCPAP) and anaplastic (8505C) thyroid carcinomas. The comparative analysis included cell behaviour assays and proteomic analysis by 2D-PAGE and mass spectrometry. IntroductionThe human thyroid gland is composed of a basic structural unit, the follicle, consisting of a monolayer of well polarized cells, the thyrocytes, responsible for the T3/T4 hormone secretion, and of other peripheral cells, the parafollicular C cells, responsible for the secretion of calcitonin. The presence within the follicle of stem cells, or remnants of embryonic cells, has been hypothesized as the target cells for tumour initiation. A thin extracellular matrix, which includes occasional fibroblasts and inflammatory cells, is peripheral to the follicle structure. Thyroid carcinomas account for 1-2% of all malignant tumours and, after those of the gonads, they represent the most common tumours of the endocrine system. The thyroid

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Section: Discussionmentioning

confidence: 99%

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

Musso

Cara

Albanese

et al. 2013

Journal of Proteomics

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“…Both FTC cell lines are derived from the same male patient and present a homozygous p53 activating mutation, whereas a homozygous phosphatase and tensin homolog inactivating mutation is only present in FTC-133 cells (Simon et al 1994, Saiselet et al 2012. FTC cell lines were purchased from the European Collection of Cell Cultures (ECACC, Salisbury, UK) and were re-authenticated by the mRNA expression profile of thyroid hormone markers and negatively analysed for mycoplasma contamination (AppliChem GmbH, Darmstadt, Germany).…”

Section: Cell Culturementioning

confidence: 99%

The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

Zwanziger¹,

Badziong²,

Ting³

et al. 2015

Endocrine-Related Cancer

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CLAUDIN-1 belongs to the family of transmembrane tight junction proteins tightening the paracellular cleft of epithelial cells. In human malignancies, CLAUDIN-1 is often dysregulated and located in subcellular compartments, particularly in the nucleus where it may influence cellular behaviour. Here, we studied CLAUDIN-1 in relation to the biological characteristics of follicular thyroid carcinoma (FTC). CLAUDIN-1 immuno-staining showed loss of membrane expression and increased nuclear CLAUDIN-1 localization in FTC metastases. CLAUDIN-1 function was further investigated in two different follicular thyroid carcinoma cell lines: FTC-133 isolated from a regional lymph node metastasis and FTC-238 derived from a lung metastasis. In both cell lines CLAUDIN-1 expression was demonstrated in the cell nuclei with a significantly higher protein expression in FTC-238 compared to FTC-133 cells. Interestingly, in vitro scratch assay revealed enriched nuclear CLAUDIN-1 expression near the scratch. Furthermore, the increase of the pathogenic character of FTC-133 cells by RASV12 transfection was associated with elevated CLAUDIN-1 expression and enhanced cell migration, invasion and proliferation. Likewise over-expression of nuclear CLAUDIN-1 in FTC-133 cells resulted in increased cell migration and invasion. Conversely, CLAUDIN-1 downregulation in FTC-238 cells by siRNA resulted in decreased cell migration and invasion and was accompanied by reduced phosphoPKC expression. Moreover, activation and inhibition of PKC resulted in CLAUDIN-1 up-and downregulation in FTC cells respectively. These data suggest an impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness, which could potentially be influenced by PKC activity.

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“…Given that this pathway is controlled by the lipid kinase activity of PTEN, the above data could be explained with the altered expression of this oncosuppressor in the two cell lines. In fact, WRO cells express WT PTEN, whereas FTC133 cells are subjected to monoallelic deletion and bear an R130STOP mutant allele for PTEN (Weng et al 2001, Saiselet et al 2012. The latter leads to a truncated PTEN isoform that is not detectable in western blotting (Fig.…”

Section: Pi3k Drives the Membrane Translocation Of Glut1 In Glucose-dmentioning

confidence: 99%

PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

Morani

Phadngam

Follo

et al. 2014

Journal of Molecular Endocrinology

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Glucose represents an important source of energy for the cells. Proliferating cancer cells consume elevated quantity of glucose, which is converted into lactate regardless of the presence of oxygen. This phenomenon, known as the Warburg effect, has been proven to be useful for imaging metabolically active tumours in cancer patients by 18 F-fluorodeoxyglucose positron emission tomography (FDG-PET). Glucose is internalised in the cells by glucose transporters (GLUTs) belonging to the GLUT family. GLUT1 (SLC2A1) is the most prevalent isoform in more aggressive and less differentiated thyroid cancer histotypes. In a previous work, we found that loss of expression of PTEN was associated with increased expression of GLUT1 on the plasma membrane (PM) and probability of detecting thyroid incidentalomas by FDG-PET. Herein, we investigated the molecular pathways that govern the expression of GLUT1 on the PM and the glucose uptake in WRO (expressing WT PTEN) and FTC133 (PTEN null) follicular thyroid cancer cells cultured under glucose-depleted conditions. The membrane expression of GLUT1 was enhanced in glucose-deprived cells. Through genetic manipulations of PTEN expression, we could demonstrate that the lack of this oncosuppressor has a dominant effect on the membrane expression of GLUT1 and glucose uptake. We conclude that loss of function of PTEN increases the probability of cancer detection by FDG-PET or other glucose-based imaging diagnosis.

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Thyroid cancer cell lines: an overview

Cited by 129 publications

References 34 publications

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

Differential proteomic and phenotypic behaviour of papillary and anaplastic thyroid cell lines

The impact of CLAUDIN-1 on follicular thyroid carcinoma aggressiveness

PTEN regulates plasma membrane expression of glucose transporter 1 and glucose uptake in thyroid cancer cells

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