Volume 9, Issue 3

Background: Thyroid-stimulating hormone receptor (TSHR) is one of the members of glycoprotein hormone receptor family; activation of TSHR by thyroid-stimulating hormone (TSH) regulates thyroid function, proliferation, and differentiation. The other family members of glycoprotein hormone receptors, such as leutinizing hormone receptor (LHR), human chorionic gonadotropin (hCG), and follicle-stimulating hormone (FSH) are known to be expressed in nonendocrine tissues including human breast cancer and regulate proliferation and differentiation. The involvement of thyroid hormones in the growth and differentiation of normal breast tissue is well documented. However, the presence of TSHR in breast cancer has not been demonstrated. The aim of the present study was to establish the expression pattern of TSHR along with transcription factors, such as octamer 4 (OCT4) and intracisternal A particle-promoted polypeptide (IPP) in human breast tumor. Materials and methods: For this study, patients with stages I–III breast cancers and adjacent noncancerous tissues were prospectively accrued and analyzed. We employed semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) and Western blot analysis to determine the expression levels of TSHR in normal and human breast cancer tissues. Results: The results indicated that a significant increase in TSHR expression was observed in tumor tissues compared to normal breast tissues. RT-PCR analysis of OCT4 and IPP also revealed a significant increase in breast tumor tissues over the controls. Conclusions: To our knowledge, this is the first report demonstrating expression of TSHR and IPP in normal breast and breast tumors. The expression of TSHR, IPP, and OCT4 increased in the human breast tumor samples over the noncancer tissues. However, further studies are needed to establish an unequivocal role for TSHR in breast tumor progression.

Successive action of cytochrome P450-7B1 (CYP7B1) and 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) on 3β-hydroxysteroids such as DHEA and epiandrosterone leads to the production of cytoprotective 7β-hydroxylated derivatives. Investigation of the presence of these enzymes in human tissues could be carried out on commercially available human tissue arrays with use of antibodies specific to CYP7B1 and 11β-HSD1 for immunohistochemistry. Both enzymes were detected mainly in tissues of endodermic and ectodermic origin which are prone to undergo inflammation. As low doses of the 7β-hydroxylated derivatives of DHEA and epiandrosterone trigger the resolution of inflammation and tissue repair, CYP7B1 and 11β-HSD1 tissue contents may reflect the tissue ability for reparation after pathological conditions.

No abstract available.