Quantitative analysis of thymosin beta-10 messenger RNA in thyroid carcinomas.
ABSTRACT Genes that are differentially expressed in benign and malignant tissues are important for the establishment of molecular-based diagnosis of carcinomas. Our recent study on the gene expression profile of thyroid carcinomas revealed an increased expression of thymosin beta-10 mRNA.
To confirm this, we measured the expression levels of thymosin beta-10 mRNA in 84 thyroid benign and malignant thyroid tissues, including five anaplastic carcinomas, by means of real-time quantitative reverse transcription-polymerase chain reaction.
We found an increased expression of thymosin beta-10 mRNA in thyroid carcinomas, especially in anaplastic carcinomas. Expression levels of thymosin beta-10 mRNA relative to thyroglobulin mRNA in anaplastic carcinomas were greatly increased compared with those in differentiated carcinomas.
These results suggest the usefulness of the quantitative measurement of thymosin beta-10 mRNA in molecular-based diagnosis of thyroid anaplastic carcinomas, but not of differentiated carcinomas.
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ABSTRACT: β-thymosins, including thymosin β4 (Tβ4), Tβ10, and Tβ15, are a family of highly conserved 5 kDa peptides. They are involved not only in normal cell migration, but also in tumor metastasis. However, the molecular mechanisms of β-thymosins to regulate cell migration and other functions are not fully understood. Recently, this important area is under active investigation worldwide. Many new discoveries have been made from molecular biology and cell culture models as well as animal models and human diseases. This timely review provides the most updated information about functional roles and molecular mechanisms of β-thymosins in normal tissues and disease conditions.Cancer Investigation 01/2013; · 2.24 Impact Factor
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ABSTRACT: Thymosin beta 10 (Tbeta10) overexpression has been reported in a variety of human cancers. However, the role of Tbeta10 in hepatocellular carcinoma (HCC) remains unclear. The aim of the present study was to analyze Tbeta10 expression in tumor and matched non-tumorous tissues, and to assess its prognostic significance for HCC after hepatectomy.World Journal of Surgical Oncology 07/2014; 12(1):226. · 1.20 Impact Factor
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ABSTRACT: Thymosin beta10 (Tbeta10) expression is associated with malignant phenotypes in many cancers. However, the role and mechanisms of Tbeta10 in liver fluke-associated cholangiocarcinoma (CCA) are not fully understood. In this study, we investigated the expression of Tbeta10 in CCA tumor tissues and cell lines as well as molecular mechanisms of Tbeta10 in tumor metastasis of CCA cell lines. Tbeta10 expression was determined by real time RT-PCR or immunocytochemistry. Tbeta10 silence or overexpression in CCA cells was achieved using gene delivery techniques. Cell migration was assessed using modified Boyden chamber and wound healing assay. The effect of silencing Tbeta10 on CCA tumor metastasis was determined in nude mice. Phosphorylation of ERK1/2 and the expression of EGR1, Snail and matrix metalloproteinases (MMPs) were studied. Ten pairs of CCA tissues (primary and metastatic tumors) and 5 CCA cell lines were studied. With real time RT-PCR and immunostaining analysis, Tbeta10 was highly expressed in primary tumors of CCA; while it was relatively low in the metastatic tumors. Five CCA cell lines showed differential expression levels of Tbeta10. Silence of Tbeta10 significantly increased cell migration, invasion and wound healing of CCA cells in vitro; reversely, overexpression of Tbeta10 reduced cell migration compared with control cells (P<0.05). In addition, silence of Tbeta10 in CCA cells increased liver metastasis in a nude mouse model of CCA implantation into the spleen. Furthermore, silence of Tbeta10 activated ERK1/2 and increased the expression of Snail and MMPs in CCA cell lines. Ras-GTPase inhibitor, FPT inhibitor III, effectively blocked Tbeta10 silence-associated ERK1/2 activation, Snail expression and cell migration. Low expression of Tbeta10 is associated with metastatic phenotype of CCA in vitro and in vivo, which may be mediated by the activation of Ras, ERK1/2 and upregulation of Snail and MMPs. This study suggests a new molecular pathway of CCA pathogenesis and a novel strategy to treat or prevent CCA metastasis.BMC Cancer 09/2013; 13(1):430. · 3.32 Impact Factor