ABSTRACT
Objective To study the expression of leukemia-related protein 16 (LRP16) in human pituitary prolactin adenomas (PRL adenomas), and the relationship between LRP16 and estrogen receptorα (ERα).Methods From October 2009 to September 2014, thirty-one adult patients diagnosed and pathologically confirmed as pituitary prolactin (PRL) adenomas (observation group) and 22 pituitary non-PRL adenomas (control group) in the Chinese PLA General Hospital were verified by the pathological examination. Immunohistochemical method was used to detect the expression levels of LRP16, PRL and ERα.Results Of the patients in observation group, those aged under 30 were predominantly females, while male patients were more common in those aged over 30. LRP16 positively existed in 26 cases (83.9%, 26/31), and ERα was positive in 28 cases (90.3%, 28/31), the both ratios were significantly higher than those in control group. ERα and LRP16 increased synchronously both in expressive content and intensity, showing a certain positive correlation between them.Conclusions Higher body mass index may be a high-risk factor badly affected the occurrence, development and prognosis in male patients with pituitary PRL; LRP16 may take part in the proliferation and formation of pituitary PRL adenomas through ERα.
ABSTRACT
Objective To investigate the effect of leukemia-related protein-16 (LRP16) gene on cell glucose uptake and its molecular mechanism.Methods LRP16 over-expression cell lines were made via translating LRP16 gene expression vector pcDNA3.1-16 and control plasmid pcDNA3.1 into 3T3-L1,C2C12,and HepG2 cell.The effect of LRP16 gene on cell glucose uptake was detected using 2-deoxy-[~3 H]-D-glucose.Western blot was used to detect the effect of LRP16 gene on the expression levels of PPARγ,GLUT-4,and GLUT 2 protein.Results Cell lines with over-expression of LRP16 gene were successfully established,the expression level of LRP16 was two fold higher than control cells.The insulin-stimulated glucose uptakes in control 3T3-L1,C2C12,and HepG2 cells were higher than cells with over-expression of LRP16 gene(P＜0.01).The expression levels of PPARγ and GLUT-4 or GLUT-2 protein in control cells were higher than cells with over-expression of LRP16 gene (P＜0.05).Conclusion LRP16 inhibits cell glucose uptake via decreasing the expression of PPARγ protein.