ABSTRACT
There are increasing evidences that HSD17B1 plays a significant role in the development of breast cancer. However, published data on the association between HSD17B1 Ser312Gly polymorphism and breast cancer risk are inconclusive. In order to derive a more precise estimation of this relationship, a meta-analysis including 9 studies with 31,053 subjects was performed in this study. Crude ORs with 95% CIs were used to assess the strength of association between HSD17B1 Ser312Gly polymorphism and breast cancer risk. The pooled ORs were performed for codominant model (Gly/Gly versus Ser/Ser, Gly/Ser versus Ser/Ser), dominant model (Gly/Gly + Gly/Ser versus Ser/Ser), and recessive model (Gly/Gly versus Gly/Ser + Ser/Ser), respectively. Overall, no significant associations were detected between HSD17B1 Ser312Gly polymorphism and breast cancer susceptibility. However, in the stratified analysis by ethnicity, significant associations were observed in Caucasians for Gly/Gly versus Ser/Ser (OR = 0.91; 95% CI 0.83-1.00), Gly/Ser versus Ser/Ser (OR = 0.92; 95% CI 0.85-0.99), and Gly/Gly + Gly/Ser versus Ser/Ser (OR = 0.92; 95% CI 0.86-0.98). In conclusion, this study suggests that HSD17B1 312Gly allele may be a protective factor for breast cancer development in Caucasians. However, large sample and representative population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding.
Subject(s)
Breast Neoplasms/genetics , Estradiol Dehydrogenases/genetics , Polymorphism, Genetic , Breast Neoplasms/enzymology , Breast Neoplasms/ethnology , Chi-Square Distribution , Female , Gene Frequency , Genetic Predisposition to Disease , Humans , Linear Models , Odds Ratio , Phenotype , Racial Groups/genetics , Risk Assessment , Risk FactorsABSTRACT
Retinoic acid (RA) is an inducer of cell differentiation. Recently, it was discovered that RA widely works on cells, causing a series of physiological alterations, and may make the tumor cell differentiation back to the normal cells, but little is known about its role in the adhesion of the cell to the extracellular matrix (Fn). We observed that RA increased the ability of NIH3T3 cells to adhere to Fn in a dose-dependent manner. The cell adhesion to fibronectin was promoted by 20% with 32 &mgr;mol/L RA, but not to polylysine. We use anti-integrin alpha(5)-subunit and beta(1)-subunit monoclonal antibodies to measure the amounts of integrin on the cell surface by FCM. It showed that the amounts of alpha(5) and beta(1) subunits of integrin did not change when the NIH3T3 cells were treated with RA for 24 h. But the incorporation of (3)H-mannose was increased by 53 % and those of tri- or tetra- antennary or bisecting complex type oligosaccharides were increased by 13 %. These results indicated that the increased adhesion of the cells to Fn in presence of RA may be caused by altering amounts and types of the oligosaccharides of the glycoprotein on the cell surface.
ABSTRACT
We have found that the binding affinity of human plasma Fn to HT1O80 cell treated with TM was 2.61x1O(-8) M, the number of binding sites was 4.24x1O(4)/cell, while those of the control group was 2.50x1O(-8) M and 2.13x1O(5)/cell respectively. These results indicate that, the Fn binding sites on the cell surface decreased by 80% after TM treatment. The binding affinity of FnR in the TM-treated cell did not alter.
