Further studies are demanded to ICG-001 decode the underlying regulatory pathways by which miRNAs participate in the carcinogenesis of bladder cancer and to identify miRNAs functioning as novel therapeutic targets or as prognostic biomarkers for bladder cancer. Some studies have reported that miR-214 was up-regulated and contributed to disease progression and distant metastases in malignant melanoma, whereas others have indicated that miR-214 was down-regulated and had a tumor-suppressive effect in cervical cancer, breast cancer and human hepatocellular carcinoma. The above evidence points out that miR-214 may play pivotal and diverse roles in oncogenesis of various tumor types, yet potential mechanisms of miR-214 are still not completely unraveled. So far, there have been little published papers involving the functional analysis and molecular network of miR-214 in bladder cancer, though a few miRNA profiling studies showed that miR-214 was dysregulated in bladder cancer. In this study, we assessed expression level of miR-214 in human bladder cancer tissues, analyzed its feasible prognostic relevance and performed relevant functional experiments. We discovered that miR-214 could inhibit bladder cancer cell proliferation, migration, invasion and exert essential proapoptotic function. Furthermore, the oncogene PDRG1 was verified for the first time as a direct downstream Cycloheximide target of miR-214 in bladder cancer. This report implicated a tumor suppressor role and regulatory mechanisms for miR-214 in bladder cancer. In the current study, we verify for the first time a vital tumor suppressor, miR-214, that functions importantly in pathogenesis of bladder cancer. miR-214 was significantly down-regulated in tumorigenic bladder cancer cell lines compared with nonmalignant immortalized bladder epithelial cell line. Attenuation of miR-214 expression was assessed in approximately 74% of bladder cancer tissues and associated with higher tumor stage, higher lymph node status, higher grade, multifocality and history of NMIBC, suggesting that miR-214 may be embroiled in cancer progression. Our data are consistent with that of several studies as follows. For instance, miR-214 suppressed growth and invasiveness of cervical cancer cells by targeting UDP-N-acetyl-��-D-galactosamine. Decreased miR-214 levels in breast cancer cells coincided with increased cell proliferation, invasion and accumulation of the Polycomb Ezh2 methyltransferase. Downregulation of miR-214 contributed to tumor angiogenesis by inducing secretion of the hepatoma-derived growth factor in human hepatoma. miR-214 regulated enhancer of zeste homolog 2 and inhibited migration and invasion in human esophageal squamous cell carcinoma. miRNA expressing profiling studies showed that miR-214 was down-regulated in malignant bladder tissue samples and significantly differentially expressed between NMIBC and MIBC. Nevertheless, miR-214 serving as oncogene had been found up-regulated in other human cancers such as ovarian, stomach, pancreatic, cervical, lung, nasopharyngeal and oral mucosal cancers and malignant melanomas. It is noticeable that functional disparities of miR-214 in different types of cancer may result from its diverse target genes or distinction among tissue types and cellular circumstances. It has been reported that miRNA can be silenced by structural genetic alterations, promoter DNA methylation and loss of histone acetylation. In addition, at least one copy of the miR-214 alleles was found to be deleted in 24% of primary breast tumors. In our study, attenuated miR-214 expression resulting from genomic loss or other mechanisms coupled with increased PDRG1 level may provide new prognostic biomarkers for the intervention of bladder cancer.