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Tytuł: The role of interactions between integrins beta1 and cyclooxygenase-2 in progression of human melanoma cells
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The aim of the study was to determine if and how β1 integrins control melanoma cells progression and if they express COX-2 as well as if there is any relation between β1 integrins and COX-2 in melanoma progression. The studies were carried out on four melanoma cell lines from various stages of cancer progression. β1 integrins expression was silenced using RNA interference method and then proliferation, apoptosis and invasion potential were analyzed. COX-2 presence was analyzed as protein expression and enzyme activity. To determine COX-2 role its activity was inhibited by specific inhibitors. β1 integrins' silencing alone had no or very weak effect on triggering apoptosis, inhibiting cells invasion and decreased proliferation in one cell line only. In analyzed cells treatment with oncological drug called Tiparnifib following β1 integrin knock out led to enhancement of apoptosis and reduction of proliferation in cells which had silenced integrin β1. All cell lines were expressing active COX-2. However, inhibition of COX-2 activity did not influenced melanoma cells survival. Suprisingly, integrin β1 silencing increased expression and activity of COX-2. To conclude, these findings suggest that β1 integrins play an important role in melanoma progression through protection against apoptosis. Surprisingly, silencing of β1 integrin alone was not sufficient to made cells enter the apop ; tosis path way but it sensitizes cells to anticancer drugs like e.g. Tipifarnib, which could be promising concept in cancer treatment. All analyzed melanoma cell lines are expressing COX-2. However, inhibition of its activity did not influence cells behaviour. There seems to be connection between integrin β1 and COX-2 in melanoma, but the mechanism is not understood at present and needs further elucidation.
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Data ostatniej modyfikacji:
17 mar 2023
Data dodania obiektu:
8 mar 2013
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http://dl.cm-uj.krakow.pl:8080/publication/3467
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| Nazwa wydania | Data |
|---|---|
| ZB-117138 | 17 mar 2023 |
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