DEXAMETHASONE DOWNREGULATES UROKINASE PLASMINOGEN ACTIVATOR (uPA) AND INHIBITS TUMOUR PROGRESSION AND METASTASIS IN MICE WITH EHRLICH MAMMARY SOLID CARCINOMA | ||||
| Egyptian Journal of Zoology | ||||
| Article 5, Volume 59, Issue 59, June 2013, Page 69-80 | ||||
| Document Type: Original Research Papers | ||||
| DOI: 10.12816/0001305 | ||||
 View on SCiNiTO | ||||
| Author | ||||
| Salwa Farouk Sabet* | ||||
| Department of Zoology, Faculty of Science, Cairo University, Giza, Egypt | ||||
| Abstract | ||||
| In many types of cancer, increased levels of the tumour-associated serine proteases uPA (urokinase-type plasminogen activator) are linked to tumour progression and metastasis. Dexamethasone (DEX) is a glugocorticoid used in the treatment of cancer and found to have inhibitory effect on cancer progression and metastasis. In the present study, we used BALB/c mice with spontaneous Ehrlich murine mammary adenocarcinoma to assess the effect of DEX on uPA gene expression and metastasis. Mice bearing Ehrlich solid carcinoma (ESC) were treated with 10 mg/kg DEX for 3, 6 and 9 days. Animals were sacrificed and ESC cells were subjected to RT-PCR and Western blot analyses to assess the uPA gene expression in term of mRNA and protein levels, respectively. To investigate metastasis occurrence in liver as secondary tumour site, liver paraffin sections were subjected to hematoxylin and eosin (H & E) staining for carcinoma cells detection. Our results revealed that: 1) uPA was overexpressed in ESC cells compared to control skeletal muscles; 2) treatment with DEX down regulated uPA expression in ESC. 3) Metastasis was observed in liver cells of mice with ESC and disappeared after treatment with DEX. We concluded that DEX treatment inhibited tumour progression and metastasis through its down regulatory effect on uPA expression. | ||||
| Keywords | ||||
| uPA; dexamethasone; Ehrlich solid carcinoma; RT-PCR; western blot | ||||
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