ACE2 was significantly increased in PTC in comparison to G, FA and UTC, and in FTC as compared to G. The ratio ACE/ACE2 decreased while ACE2/ACE increased with the differentiation grade of thyroid carcinoma.
The loss of E-CAD and expression of EMT regulators was significantly correlated with distant metastasis and vascular invasion (VI) in the well-differentiated follicular carcinoma (WD-FTC), and six tumours of metastatic sites also showed variables positive for EMT regulators.
Acting as a cell cycle repressor, IGFBP7 plays an important tumor-suppressive role in human thyroid cancer, especially in FTC and ATC subtypes and may represent a promising biomarker and therapeutic target for human thyroid cancer treatment.
HLA complex P5 (HCP5), a long non-coding RNA (lncRNA), has been shown to be implicated in several types of cancer, such as follicular thyroid carcinoma (PTC), the main type of thyroid cancer.
In this report, we show that mortalin is also upregulated in other thyroid tumor types, including papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), and anaplastic thyroid carcinoma (ATC), and that mortalin depletion can effectively induce growth arrest and cell death in human PTC (TPC-1), FTC (FTC133), and ATC (8505C and C643) cells in culture.
Two of the most highly upregulated genes, prostate cancer antigen 3 (PCA3) and HOX antisense intergenic RNA myeloid 1 (HOTAIRM1 or HAM-1), were selected for further studies using a thyroid tissue microarray(TMA) with formalin-fixed paraffin-embedded tissues of normal thyroid (NT, n = 10), nodular goiters (NG, n = 10), follicular adenoma (FA, n = 32), follicular carcinoma (FCA, n = 28), papillary thyroid carcinoma (PTC, n = 28), follicular variant of papillary thyroid carcinoma (FVPTC, n = 28), and anaplastic thyroid carcinoma (ATC, n = 10).
Although LKB1 has traditionally been considered a tumor suppressor, our data indicates that it may have a complex role in the thyroid gland, where its activation appears to be frequently associated with follicular thyroid carcinoma in both mice and humans.
Herein, we studied the role of PROX1 in angiogenesis in cell lines derived from follicular thyroid cancer (FTC: FTC-133) and squamous cell carcinoma of the thyroid gland (SCT: CGTH-W-1) upon <i>PROX1</i> knockdown.
Two of the most highly upregulated genes, prostate cancer antigen 3 (PCA3) and HOX antisense intergenic RNA myeloid 1 (HOTAIRM1 or HAM-1), were selected for further studies using a thyroid tissue microarray(TMA) with formalin-fixed paraffin-embedded tissues of normal thyroid (NT, n = 10), nodular goiters (NG, n = 10), follicular adenoma (FA, n = 32), follicular carcinoma (FCA, n = 28), papillary thyroid carcinoma (PTC, n = 28), follicular variant of papillary thyroid carcinoma (FVPTC, n = 28), and anaplastic thyroid carcinoma (ATC, n = 10).
ACE2 was significantly increased in PTC in comparison to G, FA and UTC, and in FTC as compared to G. The ratio ACE/ACE2 decreased while ACE2/ACE increased with the differentiation grade of thyroid carcinoma.
This study seeks to characterize somatostatin receptor expression in follicular thyroid cancer and anaplastic thyroid cancer and to assess the effects of somatostatin analogues.
Thyroid growth is driven by the TSH/cAMP/PKA signaling pathway, and it has previously been shown that activation of PKA through genetic ablation of the regulatory subunit Prkar1a (Prkar1a KO) is sufficient to cause follicular thyroid cancer in mouse models. cAMP also activates the Epac proteins and their downstream effectors, Rap1a and Rap1b.
Collectively, these results indicate that the rate of loss of CD56 immunohistochemistry expression was significantly higher in malignant tumors, such as papillary thyroid carcinoma and follicular carcinoma, than in follicular adenoma, benign follicular nodule, and Hashimoto's thyroiditis.
Western blot analysis in thyroid cell lines demonstrated that LIMD2 is expressed in two PTC cell lines, while it is not expressed in normal thyroid and follicular thyroid carcinoma cell lines.
We evaluated immunohistochemically the expression of hypoxia-associated proteins by hypoxia-induced factor 1α (HIF-1α), the stroma-remodeling marker Tenascin C, as well as markers for the epithelial-mesenchymal transition (EMT), namely E-cadherin and slug in a series of 59 sporadic FTCs.