We examined in this study the expression of ACE and ACE2 in thyroid tissues and their possible employment as biomarkers for thyroid cancer progression.
We examined in this study the expression of ACE and ACE2 in thyroid tissues and their possible employment as biomarkers for thyroid cancer progression.
Here, we used a panel of human thyroid cancer-derived cell lines covering the spectrum of thyroid cancer phenotypes to examine FOXE1 expression and to test for correlations between FOXE1 expression, the allele frequency of two single nucleotide polymorphisms (SNPs) and a length polymorphism in or near the FOXE1 locus associated with cancer susceptibility, and the migration ability of thyroid cancer cell lines.
In conclusion, we have identified ZEB1 as a bona fide target of FOXE1 in thyroid cancer cells, which provides new insights into the role of FOXE1 in regulating cell migration and invasion in thyroid cancer.
Thus, directed modification of CPE enables eradication of tumor entities that cannot be targeted by CPEwt, for instance Cldn1-overexpressing thyroid cancer by using the novel CPE-Mut3.
Our present findings expounded a novel signal cascade employing miR-154-3p/487-3p and RHOA to fine-tune thyroid cancer cell proliferation and apoptosis.
Low expression levels of miR-154-3p and miR-487-3p significantly correlated with tumor size, TNM stage, histological grade, lymph node metastasis and shorter overall survival in patients with thyroid cancer.
In this review, we report an overview on the biological role of HSPs, and specifically HSP90s, in thyroid cancer and their potential involvement as biomarkers.
As 17-β-estradiol (E2) has been shown to have a proliferative effect on benign and malignant thyroid cells, G protein-coupled estrogen receptor (GPER1) could have a role on the pathogenesis of thyroid cancer.
As 17-β-estradiol (E2) has been shown to have a proliferative effect on benign and malignant thyroid cells, G protein-coupled estrogen receptor (GPER1) could have a role on the pathogenesis of thyroid cancer.
In the present study, we aimed to explore the association between MALAT1 polymorphisms and thyroid cancer (TC) susceptibility, as well as potential biological function in TC.
Additionally, the expression of Bcl-2 was also enhanced in all the thyroid cancer cells and miR-15 ectopic expression could cause suppression of the Bcl-2 expression in MDA-T35 cells.
At present several clinical trials both in melanoma and thyroid cancer are using BRAF-inhibitors with encouraging results, which are derived also from numerous <i>in vitro</i> pre-clinical studies aimed at evaluate the possible modulation of immune-cell density and of specific pro-tumorigenic chemokine secretion (CXCL8 and CCL2) by several BRAF-inhibitors in the context of melanoma and thyroid cancer.
At present several clinical trials both in melanoma and thyroid cancer are using BRAF-inhibitors with encouraging results, which are derived also from numerous <i>in vitro</i> pre-clinical studies aimed at evaluate the possible modulation of immune-cell density and of specific pro-tumorigenic chemokine secretion (CXCL8 and CCL2) by several BRAF-inhibitors in the context of melanoma and thyroid cancer.
Additionally, given its role in tumorigenesis and cancer progression, galectin-3 targeting is currently under investigation for its potential utility as treatment for thyroid cancer.<b>Areas covered</b>: Recent studies of galectin-3 as a serum marker for thyroid cancer diagnosis, and in the preclinical setting as a target for cancer imaging and therapy.<b>Expert opinion</b>: Even though current studies evaluating galectin-3 as a serum marker and target for cancer imaging and therapy are promising, further research is required before it can be adopted into routine clinical use.
In conclusion, the data of this study suggested that naringin presented anti-tumor effects in TC cells through inhibiting TC cell proliferation and inducing cell apoptosis via regulating the expression of cell proliferation and apoptosis related genes and PI3K/AKT pathway activation.