| The mechanism which ionization radiation induced tumor isn't clear. To elucidate the mechanism of radiation carcinogenesis will help us to understand the tumors further, provide the scientific evidence for the prevention and treatment of tumors. Protein tyrosine phosphatase (PTPase) can dephosphorylate the phosphorylating tyrosine, which have consangnineous correlation with proliferation and differentiation of cell, and the obstacle of proliferation and differentiation is one of the tumor's characteristic. The relationship between SHP-1, SHP-2(src homology-2 domain containing PTPase) and tumor isn't still clear. And report about relationship between SHP-1, SHP-2 and radiation carcinogenesis aren't found. At first, we establish the leukemia model induced byγ-ray irradiation in mice and the malignant transformation model in BEAS-2B cell line. With the methods of PCR-single strand conformational polymorphism (PCR-SSCP), real time quantitative PCR, immunoprecipitate and Western blot, gene mutation, mRNA content, the expression and phosphorylation of protein and catalysis activity of SHP-1, SHP-2 were detected in radiation carcinogenesis. The results show that ①The leukemia model in mice and the malignant transformation model in BEAS-2B cell were successfully established, and the incidence rate of leukemia is about 36.47% in mice; ② The change of expression of SHP-1 and SHP-2 was found in the early stage afterγ-ray injury: The expression of SHP-2 in every irradiation groups was significantly higher than that of control group, and the expression of SHP-1 in 4 times irradiation groups was significantly higher than that of control group and every other irradiation groups. There were no significant differences on SHP-1 and SHP-2 between irradiation groups and control group in month 3 afterγ-ray irradiation; ③ Tyrosine phosphorylation in leukemia cell in canceration groups was higher than that in uncanceration groups and controls significantly, which were found in the protein of which molecular weight is 47.5~83×103 and close to 32.5×103 specially; ④ An obstacle to translation of SHP-1 mRNA in thymus and bone marrow cell, which expression of SHP-1 protein were increased and its mRNA content were unchanged, was found in canceration groups. At the same time, another obstacle to SHP-1, which the expression of SHP-1 protein were increased and its tyrosine phosphorylation and catalysis activity were unchanged, were also found in canceration groups; ⑤ The change of SHP-2 in thymus cell weren't the same as that in bone marrow in canceration groups: An obstacle to translation of SHP-2 mRNA in thymus cell, which expression of SHP-2 protein were increased and its mRNA content were unchanged, was found in canceration groups, and the tyrosine phosphorylation and catalysis activity of SHP-2 had the same tendency as the expression of SHP-2 protein. But there weren't more significantly change on mRNA content, expression of protein and catalysis activity of SHP-2 in bone marrow in canceration groups than in uncanceration and control groups; ⑥SHP-2 mRNA's 700~1096bp coding the PTPase catalysis domain may be methylated in canceration groups; ⑦ We detected a protein of which molecular weight is about 55×103 in canceration groups. The protein had the same antigenicity as IgG, and the change of the protein had the same tendency as SHP-2, which was higher in canceration groups than in uncanceration groups and control groups in thymus cells, but there weren't significant change in bone marrow cells; ⑧ The change law of the expression of SHP-1 and SHP-2 during γ-ray induced malignant transformation in BEAS-2B cell is that the expression of SHP-1 was increased synchronistically with malignant transformation of cell, and the expression of SHP-2 didn't have significant correlation with malignant transformation of cell.These results suggested that ①The tyrosine phosphorylation of protein has a consangnineous correlation with radiation carcinogenesis; ②SHP-1 may contribute to leukemia induced byγ-ray in mi...
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