[Expression of MIF, VEGF and p16 proteins and their correlation with clinicopathological features in cervical cancer].
OBJECTIVE
To investigate the expression of macrophage migration inhibitory factor (MIF), p16 and vascular endothclial growth factor (VEGF) proteins and their relationship with clinicopathological features in cervical cancer.


METHODS
Tissue microarray (TMA) and immunohistochemistry were used to detect the expression of MIF, p16 and VEGF proteins in specimens of 10 normal cervical epithelial tissues, 18 cervical intraepithelial neoplasia (CIN II, III) and 31 cervical squamous cell carcinomas. Western blotting was used to detect the expression of MIF, p16 and VEGF proteins in fresh samples of 3 normal cervical epithelial tissues, 3 CIN (III) and 6 cervical squamous cell carcinomas (3 Ib and 3 IIb).


RESULTS
Positive expression rates of MIF were 0, 72.2% and 93.5% in the normal, CIN and carcinoma samples, 20.0%, 33.3% and 71.0% for p16, and 10.0%, 44.4% and 74.2% for VEGF, respectively. The expression rates and levels of the three genes were significantly higher in cervical carcinomas than those in CIN. MIF expression was significantly higher in the cases with lower differentiation (17 cases, P = 0.021), and was positively correlated with VEGF expression (P = 0.0045). VEGF expression rate was significantly higher in both cases of poorly differentiated carcinomas and those with stage II b carcinoma or beyond (P = 0.004, P = 0.008). p16 expression was not found to be correlated with tumor differentiation or clinical stage. It was showed by Western blotting that the expression levels of MIF, VEGF and p16 were significantly higher in the carcinomas than those in CIN or normal tissues.


CONCLUSIONS
Expression of MIF, VEGF and p16 are probably involved in the process of cervical carcinogenesis. MIF expression is correlated with tumor differentiation. VEGF expression is correlated with both tumor differentiation and clinical stage.
Li
Wen
W
Surgical Laboratory, Department of Surgery, First Affiliated Hospital, SUN Yat-sen University, Guangzhou 510080, China.
He
Mian
M
Zeng
Jian-Fang
JF
Xia
Jin-Tang
JT
Chen
Lian-Zhou
LZ
Chen
Yang
Y
Liu
Jun-Xiu
JX
D002294:Carcinoma, Squamous Cell / Q000378:metabolism* / Q000473:pathology; D002584:Cervix Uteri / Q000378:metabolism / Q000473:pathology; D019941:Cyclin-Dependent Kinase Inhibitor p16; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000378:metabolism*; D008263:Macrophage Migration-Inhibitory Factors / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000378:metabolism*; D009367:Neoplasm Staging; D002583:Uterine Cervical Neoplasms / Q000378:metabolism* / Q000473:pathology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D002578:Uterine Cervical Dysplasia / Q000378:metabolism / Q000473:pathology
C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D008263:Macrophage Migration-Inhibitory Factors; D009363:Neoplasm Proteins; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D019746:Intramolecular Oxidoreductases; C515598:MIF protein, human