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Lung adenocarcinoma, with increased incidence in the world, exhibits poorprognosis and is usually resistant to conventional chemotherapy due to drug resistance.The enhancer of zeste homologue 2 (EZH2), a histone methyltransferase, plays akey role in tumorigenesis and cancer development through chromatin remodelingin various types of cancer. However, its potential role in lung adenocarcinomahas not been well defined. In this study, the expression of EZH2 was examinedin lung adenocarcinoma tissues and cell lines. Most interestingly, EZH2 overexpressionwas detected in tumor tissue and significantly correlated with histological differentiation,pathological tumor-node-metastasis stage and smoking history, but not with genderor age. Furthermore, EZH2 overexpression was also detected in cisplatin-resistantcancer cells rather than cisplatin-sensitive cells. Short hairpin RNA targetedagainst EZH2 inhibited cell proliferation and migration, and led to G(2)/M cellcycle arrest and apoptosis in both cisplatin-resistant and cisplatin-sensitivecell lines. Moreover, EZH2 knockdown enhanced cisplatin sensitivity of cisplatin-resistantcells and reduced the expression levels of multidrug resistance-related protein1. Our study suggests that EZH2 contributes to the progression of lung adenocarcinoma,and the deletion of EZH2 inhibits cancer and resensitizes cells to cisplatin inlung adenocarcinoma.

The expression and significance of the enhancer of zeste homolog 2 in lung adenocarcinoma