A comparative study of cell cycle mediator protein expression patterns in anaplastic and papillary thyroid carcinoma

Evans, Juanita J.; Crist, Henry; Durvesh, Saima; Bruggeman, Richard; Goldenberg, David

doi:10.4161/cbt.20560

Cited by 18 publications

(15 citation statements)

References 21 publications

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“…This pattern of distribution suggests that the ER genomic pathway and the ER nongenomic pathway may function differentially between PTC and ATC, thus possibly offering some clues regarding the different manifestations of PTC cells and ATC cells in terms of the reciprocal inhibition offered by PPARγ and ERβ. The different responses of PTC and ATC cells to the reciprocal interaction of PPARγ and ERβ are line with recent studies of both forms of thyroid cancers at the mRNA and protein levels, in which mRNA and proteomic signatures of ATC were associated much more closely with a high proliferation rate, epithelial to mesenchymal transition, invasion, dedifferentiation, glycolysis, lactate generation, and chemoresistance …”

Section: Discussionsupporting

confidence: 83%

“…The different responses of PTC and ATC cells to the reciprocal interaction of PPARg and ERb are line with recent studies of both forms of thyroid cancers at the mRNA and protein levels, in which mRNA and proteomic signatures of ATC were associated much more closely with a high proliferation rate, epithelial to mesenchymal transition, invasion, dedifferentiation, glycolysis, lactate generation, and chemoresistance. [23][24][25] Although we did not observe a direct proteinprotein interaction between ER and PPARg through coimmunoprecipitation experiments (data not shown), an indirect contact or communication between them could not be excluded. ERE, which drives the expression of the vitellogenin A2 gene, can also function as a PPRE to be bound by a PPAR/RXR heterodimer, and such a PPAR/ RXR heterodimer inhibits transactivation by the ER through competition for ERE binding.…”

Section: Discussionmentioning

confidence: 69%

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The cross‐talk between estrogen receptor and peroxisome proliferator‐activated receptor gamma in thyroid cancer

Chu

Hasselt

Vlantis

et al. 2013

Cancer

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BACKGROUND: Estrogen receptor (ER) and peroxisome proliferator-activated receptor gamma (PPARg) are associated with thyroid tumorigenesis and treatment. However, the interaction between them has not been studied. METHODS: The impact of ER overexpression or down-expression by DNA/small interfering RNA (siRNA) transfection, ERa agonists, and the ERb agonist diarylpropiolnitrile (DPN) on PPARg expression/activity was examined in papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC) cells. The effects of PPARg modulation by rosiglitazone (RTZ), a PPARg ligand, and of PPARg siRNA on ER expression were determined. Cellular functions reflected by cell proliferation and migration were assayed. Apoptosis was analyzed by terminal deoxynucleotidyl transferase dUTP nick-end labeling, and apoptotic-related proteins were evaluated by Western blot analysis. RESULTS: PPARg protein and activity were reduced by the over-expression of either ERa or ERb, whereas repression of ERa or ERb increased PPARg expression. The administration of RTZ counteracted the effects of ER and also reduced their expression, particularly in PTC cells. Moreover, knockdown of PPARg increased ER expression and activity. Functionally, ERa activation offset the inhibitory effect of PPARg on cellular functions, but ERb activation aggregated it and induced apoptosis, particularly in PTC cells. Finally, the interaction between ERb and PPARg enhanced the expression of proapoptotic molecules, such as caspase-3 and apoptosis-inducing factor. CONCLUSIONS: This study provides evidence supporting a cross-talk between ER and PPARg. The reciprocal interaction between PPARg and ERb significantly inhibits the proliferation and migration of thyroid cancer cells, providing a new therapeutic strategy against thyroid cancer. Cancer 2014;120:142-53.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 69%

The cross‐talk between estrogen receptor and peroxisome proliferator‐activated receptor gamma in thyroid cancer

Chu

Hasselt

Vlantis

et al. 2013

Cancer

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“…Inactivating TP53 mutations have been reported in about 26% of PDTC (71,73,85) and in more than 60% of UTC (42,69,70,71,73,85). The results of the studies based on the detection of nuclear accumulation of p53 protein (73,74,75,76,86,87) fit with molecular studies. p53 expression is more obvious in areas showing active infiltrative growth and/or at the periphery in PDTC, and widespread positivity for p53 is characteristic of UTC.…”

Section: Tp53 Mutationssupporting

confidence: 65%

“…All of these peculiar morphological features are characteristic of the so-called micropapillary/hobnail variant of PTC (85,86,87,88,89), an aggressive type of PTC carrying poor outcome, which is consistently positive for p53 (85,86,87,89) at the immunohistochemical level. Hobnail features were most commonly observed in association with PDTC and UTC (90).…”

Section: Tp53 Mutationsmentioning

confidence: 99%

ENDOCRINE TUMOURS: Genetic predictors of thyroid cancer outcome

Tavares

Melo

Cameselle-Teijeiro³

et al. 2016

European Journal of Endocrinology

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Genetic predictors of outcome are reviewed in the context of a disease -cancer -that can be (too) simplistically described as a 'successful, invasive clone of our own tissues'. Context has many faces that determine a thyroid cancer patient's outcome beyond the influence of genetic markers. There is also plenty of evidence on the prognostic meaning of the interplay between genetics and context/microenvironment factors (encapsulation, degree of invasion, staging, etc.). This review addresses only genetic alterations detected by molecular methods in surgically resected specimens, thus ruling out immunohistochemistry and (F)ISH, despite their crucial relevance as topographically oriented methods. For the sake of the discussion, well-differentiated carcinomas were divided into two main morphologic types: papillary carcinoma (classic and most variants) displaying BRAFV600E mutations and RET/papillary thyroid carcinoma rearrangements and the group of follicular patterned carcinomas that encompasses follicular carcinoma and the encapsulated form of follicular variant of papillary carcinoma, displaying RAS mutations and PAX8/PPARg rearrangement. TERT promoter mutations have been recently described (and associated with distant metastases and reduced survival) in papillary and follicular carcinomas, as well as in poorly differentiated and undifferentiated carcinoma. TP53 mutations, previously thought to be restricted to less differentiated carcinomas, were also detected in papillary and follicular carcinoma and found to carry a guarded prognosis. Besides their putative importance for targeted therapies, the prognostic meaning of such mutations is discussed per se and in the setting of concurrent BRAF mutation.

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“…p53 expression has been reported in various tumors, mainly in UDCs and PDCs and rarely in well-differentiated carcinomas as well as MCs in thyroid neoplasms. [220][221][222][223][224][225][226] BRAF Mutation-Specific Antibody…”

Section: Other Cell Adhesion Molecules Cell Cyclementioning

confidence: 99%