The 3 cell lines were KB-G2, an epidermal carcinoma cell line that had been transfected to overexpress mdr1 mRNA (i.e., Pgp++) compared with its parent (Pgp+) KB-31, and TCO-1, a thyroid carcinoma cell line also reported to be Pgp++.
GSEA clearly showed that the expression of OxPhos and MRP gene sets was significantly lower in primary thyroid cancer than in matched normal thyroid tissue.
We designed and synthesized targeted ABCE1-siRNA sequences and a negative control sequence (NC-siRNA), and transfected them into human thyroid cancer SW579 cells by electrotransfer to obtain ABCE1-SW579 and NC-siRNA-SW579 cells (siRNA is small interfering RNA).
In this study, we aimed to evaluate how CYP3A4/5 and ABC transporter polymorphisms affected the mean steady-state dose-adjusted plasma trough concentrations (C<sub>0</sub>) of lenvatinib in a cohort of 40 Japanese patients with thyroid cancer.
We additionally show that 8 CpG sites located within the ABI3 promoter are hypermethylated in most thyroid carcinoma samples and the degree of methylation correlated with ABI3 expression.
Taken together, these results suggest that selective suppression of c-ABL activity by STI571 may represent a potential anticancer strategy for p53-mutated undifferentiated thyroid carcinomas.
We suggest that amplification of gene(s) located at chromosome 9, other than the C-ABL, may play a significant role in anaplastic evolution of thyroid carcinomas.
The mutations activating the TSHR gene(s) in the thyroid carcinomas, were located at the codon 623 changing an Ala to a Ser (GCC-->TCC) or in codon 632 changing a Thr to Ala or Ile (ACC-->GCC or ACC-->ATC).
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.
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.
We believe this to be the first demonstration of LAR overexpression in thyroid carcinoma and may help to elucidate the role of PTPases in the development of malignancy.
We further found that a possible mechanism of Rg3 inhibiting thyroid cancer cells metastasis was associated with inhibiting cells actin skeleton function.
In a search for potential synthetic-lethal targets for FLCN using a phosphatase siRNA library screening approach, we found that knockdown of SSH2 serine phosphatase (one of the three members of Slingshot family and previously implicated in actin reorganization) specifically induced Caspase3/7 activity in a dose-dependent manner (up to six-fold increase, 10 nM, 72 h) in two human FLCN-deficient cell lines (BHD-origin renal cell carcinoma UOK257 and thyroid carcinoma FTC133) but not in their folliculin expressing isogenic cell lines.
Consistent with the above, CD97 expression in human thyroid cancers correlated with LPA receptor and markers of aggressiveness including Ki67 and pAKT.
Consistent with the above, CD97 expression in human thyroid cancers correlated with LPA receptor and markers of aggressiveness including Ki67 and pAKT.