[Cell differentiation during carcinogenesis of cervical epithelia]

The disturbance of cell differentiation is an important characteristic of tumor, but, up to date, the researches on this aspect are not as deep as those on cell proliferation of tumor. This study was to detect the alterations of cell differentiation and relative regulating factors during the carcinogenesis of cervical epithelia.

The protein expression of keratin (KT) 10, 14, 19 and beta1-integrin and beta-catenin in 20 specimens of normal squamous epithelium (NSE), 19 specimens of dysplasia squamous epithelial hyperplasia (DSEH), 39 specimens of squamous carcinoma in situ (SCIS), and 20 specimens of invasive squamous epithelial carcinoma (ISEC) were detected by inmmunohistochemistry; the mRNA expression of of beta1-integrin and beta-catenin were detected by in situ hybridization.

The strong positive rates of KT10 in NSE, DSEH, SCIS, and ISEC were 85.0%, 52.6%, 18.0% and 0, respectively, with a descending trend; it was significantly lower in SCIS and ISEC than in NSE and DSEH (Chi(2)=11.28, P<0.05; Chi(2)=8.53, P<0.05). The expression of KT14 and KT19 showed a heterogeneity in SCIS and ISEC: the proteins were negative in some cases, but overexpressed in other cases with positive cells moved upwards from the basal layer; positive cells scattered at the full epithelial layer of SCIS. The expression of beta1-integrin also showed a descending trend in NSE, DSEH, SCIS, and ISEC. The positive rate of beta1-integrin was significantly lower in ISEC than in NSE and DSEH (Chi(2)=7.62, P <0.05; value of exact probability=0.014, P < 0.05); the mRNA expression of beta1-integrin showed the same trend as its protein expression in the samples although the difference were not significant. The protein and mRNA expression of beta-catenin was located in nuclei or cytoplasm of SCIS and ISEC; increased positive cells moved upwards from the basal layer.

Restraint of terminal differentiation of epithelial cells may relate to the abnormal expression of beta1-integrin and the dysfunction of Wnt signaling pathway on regulating cell differentiation during the carcinogenesis of cervical epithelia. The expression of KT10 and beta1-integrin in SCIS is not obviously different from that in ISEC.