RESUMEN
Objective To study the expression of insulin-like growth factor-Ⅱ receptor(IGF-Ⅱ R) and its relationship with the prognosis of human epidermalgrowth factor receptor 2 (HER2) positive breast cancer.Methods The expression of IGF-Ⅱ R in 104 specimens of HER2 positive breast cancer was evaluated by immunohistochemistry.The expression was rated on 2 scales:negative and positive.The age,pathological type,tumor size,lymph node involvement,status of estrogen receptor(ER),and progesterone receptor(PR) of all the cases were reviewed.The relationship between the expression of IGF-Ⅱ R and the above pathological parameters were analyzed by statistical methods.The relationship between the expression of IGF-Ⅱ R and the disease-free survival and overall survival was studied.Results The positive expression rate of IGF-Ⅱ R was 43.3％ (45/104).The positive rate of IGF-Ⅱ R was significantly higher in the lymph node positive group than in the lymph node negative group (61.5 ％ vs 25.0％,P =0.000).No significant correlation was observed between the expression of IGF-Ⅱ R and age,pathological type,tumor size,status of ER,or PR.The disease-free survival and overall survival was significantly lower in IGF-Ⅱ R positive group than in IGF-Ⅱ R negative group.(The 5-year disease-free survival:62.6％ vs 84.7％,P =0.022; The 5-year overall survival:71.5％ vs 89.6％,P =0.024).Cox regressive analysis showed that the lymph node status was an independent risk factor of disease-free survival and overall survival,while the IGF-Ⅱ R was not.Conclusion The positive expression of IGF-Ⅱ R in HER2 positive breast cancer indicates poor prognosis.The expression of IGF-Ⅱ R may be regulated by insulin-like growth factor-Ⅱ (IGF-Ⅱ).
RESUMEN
Objective To study the growth inhibition of human hepatoma cells tranfected with type Ⅱ insulin like growth factor receptor (IGF ⅡR) antisense gene. Methods We constructed the recombinant eucaryotic expression plasmids of IGF ⅡR sense and antisense genes, which were transfected into SMMC 7721 human hepatoma cell line using calcium phosphate coprecipitation, and selected in DMEM supplemented with 500 ?g/ml G418(Geneticin) for 2～3 weeks. Then the total number of colonies formed was counted. The effect of IGF ⅡR antisense gene transfection on endogenous IGF ⅡR mRNA levels was examined by Northern blot, and the growth rate and the ability of the transfected cells to form colonies in soft agar medium were also examined. Results The hepatoma cells transfected with IGF ⅡR antisense gene exhibited significant reduction in endogenous IGF ⅡR messenger RNA(mRNA) levels and loss of their ability for anchorage independent growth in soft agar. The IGF ⅡR antisense gene supressed the formation of colonies of SMMC 7721 cells resistant to G418 without alteration on cell growth curve. Conclusion The IGF ⅡR antisense gene expression effectively blocks IGF Ⅱ to IGF ⅡR autocrine and/or paracrine signal transduction pathway and reverses certain aspects of the cell malignant phenotype.