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The FGF1/CPP-C chimera protein protects against intestinal adverse effects of Carbon-ion radiotherapy without exacerbating pancreatic carcinoma.

ABSTRACT: In order to screen for molecules contributing to the effects of FGF1/CPP-C on radiation-induced intestinal damage, the total RNA expression profile of the irradiated jejunum was obtained using a DNA microarray analysis after Carbon-ion irradiation with the FGF1/CPP-C pretreatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE113641 | GEO | 2018/11/14

REPOSITORIES: GEO

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Project description:Background and purpose:Carbon ion (C-ion) beams are concentrated to irradiate pancreatic carcinoma in the upper abdomen; however, this radiotherapy potentially causes adverse reactions in the gastrointestinal tract. FGF1 is a candidate radioprotector for radiation-induced intestinal damage, but may promote the malignancy of pancreatic cancer. An FGF1/CPP-C chimeric protein was created to enhance the intracellular signaling mode of FGF1 instead of FGFR signaling. The present study investigated the effects of FGF1/CPP-C on the intestinal adverse reactions of C-ion radiotherapy as well as its influence on the malignancy of pancreatic cancer. Materials and methods:FGF1/CPP-C was administered intraperitoneally to BALB/c mice without heparin 12?h before total body irradiation (TBI) with low-LET C-ion (17?keV/?m) at 6-8?Gy. Several radioprotective effects were examined in the jejunum. The invasion and migration of the human pancreatic carcinoma cell lines MIAPaCa-2 and PANC-1 were assessed using Boyden chambers after cultures with FGF1/CPP-C. Results:The FGF1/CPP-C treatment promoted crypt survival after C-ion irradiation at 7-8?Gy significantly more than the FGF1 treatment. FGF1/CPP-C also inhibited C-ion radiotherapy-induced apoptosis and reduced ?H2AX foci in crypt cells more than FGF1. However, FGF1/CPP-C inhibited the downstream signaling pathways of FGFRs and suppressed the activation of cell-cycle regulatory molecules in the intestine until 4?h after TBI. Furthermore, IEC6 cells were arrested in G2M after cultures with FGF1/CPP-C or FGF1, suggesting that DNA repair after irradiation is promoted by FGF1/CPP-C-induced G2M arrest. In contrast, FGF1/CPP-C appeared to be internalized into MIAPaCa-2 and PANC-1 cells more efficiently than FGF1. Therefore, FGF1/CPP-C reduced the in vitro proliferation, invasion, and migration of MIAPaCa-2 and PANC-1 cells significantly more than FGF1 through the cellular internalization of FGF1. Conclusion:These results suggest that the intracellular signaling mode of FGF1/CPP-C attenuates the intestinal adverse effects of C-ion radiotherapy without enhancing the malignancy of pancreatic carcinoma.

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The FGF1/CPP-C chimera protein protects against intestinal adverse effects of Carbon-ion radiotherapy without exacerbating pancreatic carcinoma.

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