Bcl-x gene was cloned by Boise[8] in 1993 by screening a chicken lymphocyte cDNA library using mouse Bcl-2 cDNA as the probe. Bcl-x has dual regulatory roles after activation. It is localized at 20q11.21 and a different splicing site at the 5′ terminus of its 1st mRNA exon leads to two fragments: a longer fragment Bcl-xl and a shorter fragment Bcl-xs. In recent years, expression of Bcl-x gene products (Bcl-xl and Bcl-xs)

in some tumors has been reported in domestic and foreign studies. However, the expression status in endometrial carcinoma tissue has rarely been characterized yet. Expression of Bcl-xl in endometrial carcinoma tissue and the significances Bcl-xl contains 241 amino acids and BH1-BH4 4 homologous sequences. Its sequence is 43% identical to that of Bcl-2 and their

click here functions are similar too. Bcl-xl could inhibit cell apoptosis through forming heterodimer with Bax in cytosol. Studies found that Bcl-xl could inhibit apoptosis in a Bcl-2-independent manner. It could inhibit cell apoptosis mediated by many apoptosis-inducing factors, which was far upstream in regulation of apoptosis. Bcl-xl protein was highly expressed Small molecule library ic50 in some tumors with low level of Bcl-2. Some researchers believed that Bcl-xl protein might have substituted the function of Bcl-2 in some tumors. Under certain condition, this protein has stronger apoptosis-inhibitory effect over Bcl-2, indicating the key role of Bcl-xl in the process of cell transformation. Studies showed that tumor cell apoptosis could be induced by lowering the Bcl-xl expression in human prostate cancer tissue[9]. Furthermore, Methocarbamol researches demonstrated that induction of tumor cell apoptosis could be achieved through inhibiting the expression of Bcl-xl in malignant pleural mesothelioma[10]. Boehmdenf et al. [11]also showed that Bcl-xl expression in head and neck squamous cell carcinoma was significantly different among different types of pathological grading, while the expression of Bcl-xl protein in human prostate cancer specimens was closely correlated with the Gleason scoring

and metastasis of human prostate cancers[12]. Therefore, Bcl-xl plays an important role in pathogenesis of tumor as an anti-apoptotic factor, and chemotherapy-resistance of the tumor cell may be associated with high level of Bcl-xl expression [13, 14]. Our study found that expressions of Bcl-xl mRNA and protein were slightly increased in simple hyperplasia and atypical hyperplasia endometrial tissues, while significantly increased in endometrial carcinoma tissue. In addition, Bcl-xl expression was correlated with the pathological grading of endometrial carcinoma, suggesting that elevation in Bcl-xl disrupted the regulation of signal transduction and normal gene expression, while it led to abnormal endometrial cell proliferation differentiation and eventually endometrial carcinoma.