Hypothyroidism Enhances Tumor Invasiveness and Metastasis Development
نویسندگان
چکیده
BACKGROUND Whereas there is increasing evidence that loss of expression and/or function of the thyroid hormone receptors (TRs) could result in a selective advantage for tumor development, the relationship between thyroid hormone levels and human cancer is a controversial issue. It has been reported that hypothyroidism might be a possible risk factor for liver and breast cancer in humans, but a lower incidence of breast carcinoma has been also reported in hypothyroid patients METHODOLOGY/PRINCIPAL FINDINGS In this work we have analyzed the influence of hypothyroidism on tumor progression and metastasis development using xenografts of parental and TRbeta1-expressing human hepatocarcinoma (SK-hep1) and breast cancer cells (MDA-MB-468). In agreement with our previous observations tumor invasiveness and metastasis formation was strongly repressed when TRbeta-expressing cells were injected into euthyroid nude mice. Whereas tumor growth was retarded when cells were inoculated into hypothyroid hosts, tumors had a more mesenchymal phenotype, were more invasive and metastatic growth was enhanced. Increased aggressiveness and tumor growth retardation was also observed with parental cells that do not express TRs. CONCLUSIONS/SIGNIFICANCE These results show that changes in the stromal cells secondary to host hypothyroidism can modulate tumor progression and metastatic growth independently of the presence of TRs on the tumor cells. On the other hand, the finding that hypothyroidism can affect differentially tumor growth and invasiveness can contribute to the explanation of the confounding reports on the influence of thyroidal status in human cancer.
منابع مشابه
E-Cadherin in Relation with the Proliferating Cell Nuclear Antigen of the Bilharzia Associ-ated and Non-Associated Urinary Bladder Carcinoma
Background: E-cadherin is a trans-membrane glycoprotein that plays a critical role in many aspects of cell adhesion as well as establishment and maintenance of epithelial cell polarity. Loss of the adhesive function of E-cadherin seems to promote invasive and metastatic properties of neoplastic cells. Objectives: The present study is a retrospective study aiming to evaluate the loss of E-cadher...
متن کاملAuthor's response to reviews Title: Berberine enhances inhibition of glioma tumor cell migration and invasiveness mediated by arsenic trioxide via the inactivation of protein kinase C Authors:
متن کامل
Igf2bp1
The oncofetal RNA-binding protein IGF2BP1 (IGF2 mRNA binding protein 1) controls the cytoplasmic fate of specific target mRNAs including ACTB and CD44. During neural development, IGF2BPs promote neurite protrusion and the migration of neuronal crest cells. In tumor-derived cells, IGF2BP1 enhances the formation of lamellipodia and invadopodia. Accordingly, the de novo synthesis of IGF2BP1 observ...
متن کاملEpithelial-to-mesenchymal transition and ovarian tumor progression induced by tissue transglutaminase.
Tissue transglutaminase (TG2), an enzyme that catalyzes Ca(2+)-dependent aggregation and polymerization of proteins, is overexpressed in ovarian cancer cells and tumors. We previously reported that TG2 facilitates tumor dissemination using an i.p. xenograft model. Here we show that TG2 modulates epithelial-to-mesenchymal transition (EMT), contributing to increased ovarian cancer cell invasivene...
متن کاملThe Effect of Interval Training on the Expression of Tumor Suppressor Gene, Systemic Inflammation, and Tumor Volume in Breast Cancer–Bearing BALB/c Mice
Introduction: E-cadherin is expressed in most normal epithelial tissues. Loss of E-cadherin can cause dedifferentiation and invasiveness in human carcinomas, leading E-cadherin to be classified as a tumor suppressor. Therefore, the aim of this study was to investigate the effect of interval training on the expression of tumor suppressor gene E-cadherin in breast cancer-bearing BALB/c mice. Meth...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره 4 شماره
صفحات -
تاریخ انتشار 2009