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  • In human cancers it has been identified that FOXC AS


    In human cancers, it has been identified that FOXC2-AS1 functions as an oncogenic RNA. For instance, in osteosarcoma, FOXC2-AS1 regulates the expression of FOXC2 at the transcription and post-transcription levels to promote doxorubicin resistance by facilitating ABCB1 expression (C.L. Zhang et al., 2017). In this study, we found that FOXC2-AS1 expression abundance was dramatically up-regulated in the clinical samples and O-1602 australia of prostate cancer. More than that, the high-expression of FOXC2-AS1 indicated the poor prognosis of prostate cancer patients, signifying the oncogenic risk factors of ectopic FOXC2-AS1for the prostate cancer patients. Being similar to the previous research, our finding also evidences the truth that FOXC2-AS1 functions as a cancer promoting molecular in the human tumors. In the prostate cancer carcinogenesis, numerous lncRNAs have been identified to modulate it through ceRNA mechanism (Liu et al., 2016; Zhang et al., 2016; Li et al., 2017; Liu et al., 2017; S. Zhang et al., 2017). For instance, lncRNA MALAT1 expression was up-regulated in docetaxel resistant prostate cancer samples, and miR-145-5p targets the MALAT1 and AKAP12, involving in DTX-resistance of cells (Xue et al., 2018). Moreover, lncRNA RNCR3 is closely associated with the poor survival and prognosis for prostate cancer patients, and mechanically binds with miR-185-5p and serves as novel biomarker (Tian et al., 2018). For another example, lncRNA SNHG7 expression is up-regulated in prostate cancer tissue and SNHG7 knockdown markedly inhibited prostate cancer proliferation and cycle-related protein (CDK4, CDK6, Cyclin D1), promoting the prostate cancer tumorigenesis via miR-503/Cyclin D1 pathway (Qi et al., 2018). EZH2 is found to be a gene signature involved in prostate cancer via the assay of collocation of EZH2 and JMJD3 on gene promoters dependent on disease stage, which may help identify diagnostic and therapeutic targets in prostate cancer (Daures et al., 2018).
    Conflict of interest
    Introduction Extranodal NK/T-cell lymphoma, nasal type (ENKTL), is an aggressive malignancy with a poor prognosis [1], [2]. It is particularly prevalent in Asian countries and parts of Latin America. Although chemotherapy and radiotherapy help improve the disease outcome, the prognosis of NKTCL remains poor [2]. There is an urgent need for effective targeted therapy. Recently, the combination of genomic and functional analysis has identified some candidate tumor suppressor genes in ENKTL, such as PRDM1, HACE1, AIM, and FOXO3 [3], but none of them are O-1602 australia an independent prognostic factor for this disease [4]. Gene expression profiling studies also have identified a number of oncogenes and signaling pathways, with differential expression and activation in ENKTL [1], [5]. However, few aberrant molecules contribute to ENKTL pathogenesis and can potentially serve as therapeutic targets. Thus, a novel diagnostic molecular predictor of tumor behavior is currently required to help guide therapeutic decisions. Enhancer of zeste homolog 2 (EZH2) is an H3K27-specific histone methyltransferase, which plays a key role in the epigenetic maintenance of repressive chromatin mark. EZH2 protein must partner with other noncatalytic proteins, such as EED and SUZ12, to form the polycomb repressive complex 2 (PRC2) to carry out its histone methyltransferase activity [6]. When the PRC2 complex is recruited to chromatin, EZH2 induces H3K27 dimethylation and trimethylation (H3K27me2/3). H3K27me3 is frequently associated with gene repression, and it is a critical epigenetic event during tissue development [7]. EZH2 has been shown to be frequently overexpressed in various human cancers including lymphoma [8], and its overexpression is associated with invasive growth and poor clinical outcomes in solid tumors such as prostate, breast, gastric, and endometrial cancers [9], [10], [11]. Very few studies have suggested that EZH2 is overexpressed in NK/T-cell lymphoma [12]. However, the relationship between EZH2 and H3K27me3 remains unclear, and their effect on prognosis has not been reported. In our study, we demonstrated that EZH2 and H3K27me3 were aberrantly overexpressed in most ENKTL, and both had important clinicopathological significance. We discovered that EZH2 overexpression was inversely associated with H3K27me3, and there is an opposite effect in clinicopathological significance and prognosis. In addition, we found that JAK3 inhibitor may reduce the growth of ENKTL cells by decreasing EZH2 expression and increasing H3K27me3 expression. Our findings may provide new ideas for the prognosis and treatment of ENKTL.