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• W2014328894 abstract "Ionizing radiation rapidly induces Panc-1, MiaPaCa, and BxPC-3 human pancreatic cancer cell invasion, which is mediated by the alpha5 beta1 integrin fibronectin receptor (FnR). Here, we report the effects of radiation on the levels and localization of alpha5 beta1 integrin, and on early and late endosomes. Adherent Panc1, MiaPaCa, and BxPC-3 cells were irradiated once with 2 Gy (Panc1) or 3 Gy (MiaPaCa and BxPC-3). One hour later, fluorescent immunostaining was performed with anti alpha 5 antiserum (Ab), P1D6 anti alpha 5 beta 1 monoclonal antibody (MAb), anti EEA-1 MAb, or anti LAMP-1 Ab. Panc1 and BxPC-3 tumors in nude mice received 2 Gy on each of 5 days before excision. Frozen sections were bound to fluorescent anti alpha 5 Ab, P1D6 anti alpha5 beta1 MAb, anti EEA-1 MAb, or anti LAMP-1 Ab. Immunofluorescence quantitation of adherent cells and sectioned tumors was performed by confocal microscopy. Radiation caused a rapid upregulation of surface alpha5 beta1 integrin FnR in Panc-1, MiaPaCa, and BxPC-3 cells. The subcellular localization of alpha5 beta1 also changed significantly: a rapid transition from low cytoplasmic perinuclear levels in unirradiated BxPC-3, MiaPaCa, and Panc-1 cells to high membrane levels shortly after radiation. Consistent results were obtained in nude mice bearing BxPC-3 and Panc1 tumors. Frozen sections of unirradiated tumors, immunostained with fluorescent anti alpha5 beta1 and anti MMP 1 Abs, showed only low levels of perinuclear alpha 5 beta 1 and MMP 1; while cells of irradiated tumors had high membrane levels of both proteins. Radiation-induced alpha5 beta1 upregulation may occur via recycling through early endosomes, a direct, short receptor recycling pathway. Alternatively, radiation-induced alpha5 beta1 upregulation may involve recycling through late endosomes, an indirect, longer receptor recycling pathway involving association with the trans-Golgi network. Our results suggest that radiation-induced alpha5 integrin upregulation in Panc1 cells occurs exclusively through increased rates of receptor recycling through early endosomes, without increased alpha5 gene transcription. Our results also show that alpha5 beta1 upregulation in MiaPaCa and BxPC-3 cells is due to increased trafficking through late endosomes, as well as increased alpha5 transcription, since RT-PCR analysis of irradiated MiaPaCa and BxPC-3 cells showed a 3- to 5-fold induction of alpha 5 mRNA. In MiaPaCa cells, radiation-induced alpha5 beta1 upregulation appears to involve increases in both early and late endosomal trafficking; while in BxPC-3 cells, radiation-induced alpha5 beta1 upregulation appears to involve late endosomal trafficking almost exclusively." @default.
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• W2014328894 date "2009-11-01" @default.
• W2014328894 modified "2023-09-27" @default.
• W2014328894 title "Radiation-induced Alpha5 Beta1 Integrin Upregulation on the Surfaces of Pancreatic Cancer Cells Involves Increased Trafficking in Early and/or Late Endosomes" @default.
• W2014328894 doi "https://doi.org/10.1016/j.ijrobp.2009.07.1235" @default.
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