Src-homology protein tyrosine phosphatase-1 (SHP-1) is a protein tyrosine phosphatase that is implicated in the regulation of growth, differentiation, survival, apoptosis and proliferation of hematopoietic cells and other cell types. Here, we found that SHP-1 is involved in regulation of early embryonic development. Embryos overexpressing SHP-1 were mainly arrested at the 8-cell stage, and Nanog mRNA expression was first observed in the morulae that showed down-regulation of SHP-1. These results suggested an antagonistic relationship between SHP-1 and Nanog during early embryonic development. Next, the specific mechanism was examined in mouse F9 embryonal carcinoma cells. We confirmed that signal transducer and activator of transcription 3 (STAT3) was a substrate for SHP-1 by co-immunoprecipitation. Using overexpression and knockdown strategies, we found that SHP-1 participated in regulation of Nanog expression. Furthermore, site mutation of STAT3 was performed to confirm that SHP-1 was responsible for rapid STAT3 dephosphorylation and a decrease of Nanog expression in F9 cells. These findings suggest that SHP-1 plays a crucial role during early embryonic development. Thus, SHP-1 may function as a key regulator for Nanog that specifically demarcates the nascent epiblast, coincident with the domain of X chromosome reprogramming.
Objective: The rabbit VX2 bone tumor model is an ideal experimental animal model for studying malignant bone tumors, but few studies on cytokines and tumor proliferation. This paper is aimed to study the effect of interferon-γ (IFN-γ) and interleukin-4 (IL-4) on the expression of proliferating cell nuclear antigen (PCNA) in tumor tissue. Methods: The experiment included 30 Japanese white rabbits divided into an experimental group (n=15) and a control group (n=15) according to the random number method. Peripheral blood and tumor tissue were collected at 1 and 2 weeks after tumor implantation. We used enzyme-linked immunosorbent assay to detect the expression levels of IFN-γ and IL-4 in peripheral blood and PCNA in tumor tissue. After the rabbits were euthanasia, the tissues were taken for pathological examination. Results: After tumor implantation, the expression level of IFN-γ in the experimental group in the 2nd week was significantly lower than that in the 1st week and 2nd week in the control group (p-value<0.005). In contrast, the expression level of IL-4 in the experimental group in the 2nd week was significantly higher than that in the 1st week and 2nd week in the control group (p-value<0.005). The expression level of PCNA in the experimental group in the 2nd week was significantly higher than that in the 1st week (P<0.005), and the PCNA expression in the 1st and 2nd week in the experimental group was higher than that in the 1st and 2nd week in the control group (p-value<0.005). In the 1st and 2nd week of tumor implantation, the correlation between IFN-γ and PCNA was negatively correlated(r=-0.566, p-value=0.028; r=-0.604, p-value=0.017), while the correlation between IL-4 and PCNA was positively correlated(r=0.583, p-value=0.023; r=0.884, p-value<0.005). Conclusion: In the VX2 bone tumor model of rabbit, with the extension of time after tumor implantation, there was a negative correlation between IFN-γ and PCNA and a positive correlation between IL-4 and PCNA.
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