MicroRNA (miR)-101 copy loss is an early event in the development of human lung cancer, and it occurs in 29% of all lung cancer incidences. In addition, miR-101 expression in non-small cell lung cancer (NSCLC) is known to be downregulated. The aim of the present study was to explore the roles and mechanisms of the long non-coding (lnc)-RNA pro-transition associated RNA (PTAR) on NSCLC cell proliferation, migration and invasion in association with miR-101. Reverse transcription-quantitative PCR analysis was performed to detect the expression of lncRNA PTAR in 30 paired human NSCLC tissues and the corresponding para-tumor tissues. PTAR was amplified and cloned into the expression vector pCDNA3.1. Then, PTAR-overexpression plasmids or small interfering (si)-RNA-PTAR was transfected into A549 cells for 48 h, after which cell proliferation and the cell cycle distribution were evaluated. In addition, Transwell chamber and cell scratch-wound assays were conducted to analyze A549 cell migration and invasion. A luciferase activity assay was evaluated to determine the interaction between PTAR and miR-101. Furthermore, our results demonstrated that in human NSCLC tissues and cell lines, lncRNA PTAR expression was upregulated compared with normal lung tissues and cell lines, respectively. Additionally, PTAR transfection was observed to promote A549 cell proliferation, migration and invasion; opposing effects were observed with siRNA-PTAR transfection. The luciferase activity assay revealed that PTAR could act as a sponge to bind miR-101. Thus, miR-101 plays a role in NSCLC tumorigenesis and progression. In conclusion, lncRNA PTAR was proposed to promote NSCLC cell growth through sponging and inactivating miR-101, which may be a possible mechanism underlying miR-101 copy loss in human NSCLC.

Abstract. Rnf2 is a fundamental component of the polycomb repressive complex 1and acts as the really interesting new gene finger E3 ligase, which is responsible for histone 2A modification. Previous studies have shown that the ring finger protein 2 (Rnf2) is overexpressed in various types of tumor and has a close association with tumor development. However, few studies have been carried out into the expression and biological function of Rnf2 in gastric cancer cells. The present study measured the expression of Rnf2 in gastric cancer cells and normal epithelial gastric cells. The results demonstrate that Rnf2 is upregulated in gastric cancer cells. In addition, the knockdown of Rnf2 inhibited the cell viability and induced increased G1 phase followed by a substantial reduction of the G2/M phase. The expression levels of p21 and p27 were also significantly elevated by the knockdown of Rnf2. These results provide evidence of the oncogenic function of Rnf2 in gastric cancer, possibly through an inhibition of cellular proliferation and a delay of the G2/M phase. Therefore, Rnf2 may be a novel target for the prognosis and therapy of gastric cancer. IntroductionPolycomb group (PcG) proteins are epigenetic regulators for gene silencing at the transcription level, acting as important regulators of DNA repair, proliferation, embryonic differentiation and cell-fate maintenance during development and in adult tissue homeostasis (1-3). These proteins exist in at least two biochemically and functionally distinct PcG core complexes referred to as polycomb repressive complex (PRC) 1 and 2. PRC2, which is involved in the initiation of gene repression, mediates the trimethylation of histone H3 at Lys27 (H3K27me3) and consists of histone methyltransferase enhancer of zeste homolog 2 (EZH2), the polycomb repressive complex and embryonic ectoderm development (4,5). The mammalian PRC1, which is an ubiquitin E3 ligase complex, consists of polycomb (PC), polyhomeotic (PH), BMI1, ring finger protein (Rnf) 1A and 2 (Rnf2) (6), among which Rnf2 has been identified as the catalytic subunit (7). Rnf2, acts as the RING finger E3 ligase responsible for H2A modification in the PRC1 complex and influences early development and embryonic stem cell maintenance as well as cancer development (8,9). Recent evidence showed that Rnf2 is highly expressed in various types of tumor in comparison to normal tissue counterparts (10). Knockdown of Rnf2 in HeLa cells resulted in morphological changes and an inhibition of cellularproliferation (7), suggesting an oncogenic function of Rnf2. Additionally, it has been reported that Rnf2 can either directly or indirectly target a distinct, specific pathway involved in cell cycle control (11,12). However, in order to acquire a complete understanding of the mechanisms through which cancer progression is regulated by Rnf2, additional investigation is required.Normal cell cycle progression is tightly controlled by a variety of molecular checkpoints, which supervise the biological processes that take place in different...

Nucleophosmin/B23 and CRM1 are molecular markers which play an important role in tumorigenesis and tumor progression in gastric cancer (GC). However, the association between the two remains unclear. This study evaluated the expression and the correlation of B23 and CRM1 in GC. B23 and CRM1 expression in GC and adjacent noncancerous tissues (ANCT) of gastrectomy specimens from 131 GC patients was measured by immunohistochemistry. Positive expression rates of B23 and CRM1 were significantly higher in GC tissues than in ANCT. The high expression rates of B23 and CRM1 were significantly higher in patients with more advanced tumor stages and distant metastasis (all p < 0.05). Only high expression of CRM1was correlated with positive Her2 status (p = 0.01). B23 expression was positively correlated with CRM1expression in GC tissues (p = 0.038). Univariate analysis showed that TNM stage (p = 0.0001), metastasis (p = 0.027), B23 (p = 0.0111), and CRM1 expression (p = 0.0019) were significant risk factors affecting overall survival. Both high expression of B23 and CRM1 in GC patients suggests poor prognosis, co-expression of the two (p = 0.043) even worse. Cox multivariate analysis showed that positive B23 (p = 0.0231) and CRM1 (p = 0.0048) expression were both independent prognostic factors that negatively correlated with survival. We revealed the co-expression of B23 or CRM1 in GC. The expression levels of B23 or CRM1 were closely related to poor prognosis in GC, and both B23 or CRM1 were independent risk factor.