Combined aberrant expression of Bmi1 and EZH2 is predictive of poor prognosis in glioma patients.

Bmi1 and EZH2 are involved in tumorigenesis of gliomas. However, clinicopathologic significance of their expression in gliomas is unknown; especially, the prognostic value of combined expression of Bmi1 and EZH2 has not been explored. Bmi1 and EZH2 expression in human gliomas and nonneoplastic brain tissues was measured by immunohistochemistry. Both Bmi1 and EZH2 expressions in glioma tissues were significantly higher than those in corresponding nonneoplastic brain tissues (both P<0.001). Additionally, the upregulations of Bmi1 and EZH2 proteins were both significantly associated with advanced WHO grades (both P<0.001) and low KPS (P=0.008 and 0.01, respectively). Moreover, the overall survival of patients with high Bmi1 protein expression (P=0.006) or high EZH2 protein expression (P=0.01) was obviously lower than those with low expressions. More interestingly, glioma patients with combined overexpression of Bmi1 and EZH2 proteins had the shortest overall survival (P<0.001). Furthermore, multivariate analysis showed that Bmi1n expression (P=0.02), EZH2 expression (P=0.03), and combined expression of Bmi1 and EZH2 (P=0.008), were all independent prognostic factors for overall survival in glioma patients. Our data suggest for the first time that the combination of Bmi1 and EZH2 overexpression may be a highly sensitive marker for the prognosis in glioma patients.

Wu Z ，Wang Q ，Wang L ，Li G ，Liu H ，Fan F ，Li Z ，Li Y ，Tu Y ... -  《-》

Distinctive expression of the polycomb group proteins Bmi1 polycomb ring finger oncogene and enhancer of zeste homolog 2 in nonsmall cell lung cancers and their clinical and clinicopathologic significance.

Kikuchi J ，Kinoshita I ，Shimizu Y ，Kikuchi E ，Konishi J ，Oizumi S ，Kaga K ，Matsuno Y ，Nishimura M ，Dosaka-Akita H ... -  《CANCER》

Co-expression of Bmi1 and EZH2 as an independent poor prognostic factor in esophageal squamous cell carcinoma.

Bmi1 polycomb ring finger oncogene (Bmi1) and the enhancer of zeste homolog 2 (EZH2) are members of polycomb repressive complex (PRC) 1 and PRC2, respectively. PRC1 represses tumor suppressor genes such as p16INK4a and p14ARF in a PRC2-dependent manner. There have been few studies on Bmi1 or EZH2 expression in esophageal squamous cell carcinoma (ESCC). We investigated Bmi1 and EZH2 expression in 164 cases of ESCCs using immunohistochemistry, and evaluated the correlation with clinicopathologic features and their prognostic significance. Bmi1 and EZH2 were more highly expressed in tumor than in adjacent normal tissue (p<0.001). High expression of Bmi1 or EZH2 alone was not correlated with any clinicopathologic parameter and did not influence the prognosis. However, the group with high expression of both Bmi1 and EZH2 showed the poorest prognosis in overall survival (p=0.027) and disease-free survival (p=0.007). Also, it was an independent prognostic factor in overall survival (p=0.047). High expression of both Bmi1 and EZH2, not each alone, is an independent poor prognostic factor in ESCCs, supporting the repression of tumor suppressor gene by Bmi1 in an EZH2-dependent manner. This result suggests that both Bmi1 and EZH2, not each alone, could be potent candidates of new target therapy in ESCCs.

Ha SY ，Kim SH 《-》

Aberrant expression of EZH2 is associated with pathological findings and P53 alteration.

Shiogama S ，Yoshiba S ，Soga D ，Motohashi H ，Shintani S ... -  《-》

Functional roles of enhancer of zeste homolog 2 in gliomas.

Gliomas are the most common and lethal type of primary malignant brain tumor. Due to the infiltrative nature and high resistance to standard first line treatment with combinations of radiation and chemotherapy, the prognosis of patient is very poor. Recently, accumulated evidence suggests that enhancer of zeste homolog 2 (EZH2) serves as an oncogene and is involved in multiple glioma cell processes, including cell cycle, invasion, glioma stem cell maintenance, drug and radiotherapy resistance and so on. In this review, we will focus on updating current knowledge of EZH2 in gliomas. Moreover, the regulation of EZH2 by microRNAs and long non-coding RNAs and the therapeutic strategies targeting EZH2 for gliomas will also be discussed.

Yin Y ，Qiu S ，Peng Y 《-》