| Objective：Chemotactic factor12(stromal cell derived factor1) and itsreceptor CXCR4play key role in tumor infiltration, diffusion and transfusion.Recently, CXCR7was identified as a novel replacement receptor of CXCL12,CXCL11I-(TAC),which is independent of CXCR4. CXCR7is made up ofseven trans-membrane RDC1gene encoding protein. CXCR7expressed inmany tumor cells. Such as Lung cancer, breast cancer, cervical cancer, kidneycancer, rhabdomyo sarcoma, prostate cancer and so on. CXCR7also exists innewborn blood vessels of tumor. Because studies show that chemokinesCXCL12and its receptor CXCR4expressed in human brain glioma tissues,CXCL12and its receptor CXCR7in other tumors were also found and withhigh expression. So we believed that chemotactic factor CXCL12and itsreceptor CXCR7expressed in human brain glioma, and began experimentalresearch. In tumor tissue, CXCR7highly expressed in tumor vascularendothelial cells, microglia and glioma cells, however, CXCR4expression ismore limited. And common expression of chemokines CXCL12and CXCR7is obvious. expression of CXCR7positively correlated with malignantdegree of gliomas. Relevant studies show that CXCR7is higher than that ofCXCR4expression when the common expression of CXCR4and CXCR7.And recent studies show that chemokines CXCL12and its receptor CXCR4exist and high expression in brain gliomas. So we believe CXCR7to be a newresearch direction, do the research of chemotactic factor CXCL12and itsreceptor CXCR7in human brain gliomas in the expression of glial cell tumorgrowth, infiltration, diffusion, transfer,which is of vital significance guidingclinical treatment and prognosis. The study was to explore expression and itsclinical significance of chemotactic factor CXCL12and its receptor CXCR7in all levels of the brain glial cell tumor. Method: we retrospectively reviewed80patients of Glial cell tumor,who received surgery to remove cancerous tissue from the second and forthhospital of hebei medical university from Feb2012to Dec2012(By the worldhealth organization (WHO) classification of standards, the Ⅰ and Ⅱ brainglioma cells were divided to low level group, the Ⅲ and Ⅳ brain gliomaswere divided to high level group.40cases of brain gliomas in low level groupand40cases of brain gliomas in high level group). The non brain gliomaspatients (no distinguish of gender)20cases of surgically resected brain tissuesas control group. Both immediately fixed and properly kept after operationwith formalin. Expression of CXCR7, CXCL12in protein level weredetected using immune-histo-chemical method.Result:1The relationship between CXCR7and glioma.A total of80cases of brain glioma group, the average rank is57.78, thesecond rank is4622.00; control group a total of20cases, of which the averagerank is21.40, second rank is428.00.（Table3）The Mann-Whitney Ustatistics is218.000; Wilcoxon W statistics is428.000; Z=-5.321, bilateraltest P=0.000.(Table4)According toα=0.05level, we think that in thegliomas group and normal control group，CXCR7expression intensitydifference was statistically significant, and CXCR7expression in gliomasgroup was obviously higher than that of normal control group.2The relationship between CXCL12and glioma.A total of80cases of brain glioma group, the average rank is54.75, thesecond rank is4380.00; control group a total of20cases, of which the averagerank is33.50, second rank is670.00.(Table5).The Mann-Whitney Ustatistics is460.000; Wilcoxon W statistics is670.000; Z=-3.082, bilateraltest P=0.002.(Table6)According toα=0.05level, we think that in thegliomas group and normal control group，CXCL12expression intensitydifference was statistically significant, and CXCL12expression in gliomasgroup was obviously higher than that of normal control group. 3The relationship between CXCR7and glioma levels.Pearson Chi-Square χ~2=64.162,df=6,P=0.000,Linear-by-Linear Associat-ion χ~2=36.357， df=1， P=0.000,(Table7)linear regression weight havestatistical significance.So we think that CXCR7expression intensity and thegliomas grade are not only related to the linear relationship. Combined withtable1,we suggests CXCR7expression intensity increased with the increasingof gliomas grade.4The relationship between CXCL12and glioma levels.Pearson Chi-Square χ~2=22.805,df=6,P=0.001,Linear-by-Linear Associati-on χ~2=17.766,df=1,P=0.000,(Table8)linear regression weight have statisticalsignificance.So we think that CXCL12expression intensity and the gliomasgrade are not only related to the linear relationship. Combined with table2,wesuggests CXCL12expression intensity increased with the increasing ofgliomas grade.Conclusion:1Expression intensity of CXCR7both in human brain glioma group andthe control group are of statistically difference, glioma group is significantlyhigher than the control group, which signal that CXCR7exist in brain gliomasand perform high expression.2Expression of CXCR7in both low level and high level brain gliomagroups are of statistically difference, expression in high level brain gliomagroup is higher than that in low level brain glioma group, which signal thatCXCR7increases with the level of brain gliomas, and positively associatedwith the degree of brain malignant glioma.3Expression intensity of CXCL12both in human brain glioma group andthe control group are of statistically difference, glioma group is significantlyhigher than the control group, which signal that CXCL12exist in braingliomas and perform high expression.4Expression of CXCL12in both low level and high level brain gliomagroups are of statistically difference, expression in high level brain gliomagroup is higher than that in low level brain glioma group, which signal thatCXCL12increases with the level of brain gliomas, and positively associated with the degree of brain malignant glioma.5Expression of CXCL12/CXCR7being of guiding significance forclinical treatment,which may effect as a predictor and be help for evaluationof the treatment, and may become the new therapeutic targets. |
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