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Background: Bladder cancer (BC) is one of the most common malignant tumors in the urinary system. Long non-coding RNA (lncRNA) plays an important role in BC. Methods: LINC00662 expression was identified by quantitative real-time polymerase chain reaction (qPCR) and in situ hybridization (ISH). The effect of LINC00662 on cell proliferation, apoptosis, migration and invasion was measured by CCK8 assay, colony formation assay, transwell assay, and western blot. Dual-luciferase reporter gene assay, RNA pull-down and RIP assay confirm the interaction between LINC00662 and miR-195-5p/VEGFA. The in vivo effect of LINC00662 on BC was investigated using a mouse tumorigenicity model. Results: LINC00662 was overexpressed in BC tissues and cell lines, and negatively correlated with the survival of BC patients. Overexpression of LINC00662 promoted proliferation, migration and invasion and inhibited apoptosis of BC cells, and LINC00662 knockdown abrogated this effect. Silencing LINC00662 inhibited BC growth in a subcutaneous BC tumor mouse model. LINC00662 acted as an oncogene through regulating miR-195-5p/VEGFA axes. Decreased VEGFA expression caused by LINC00662 knockdown inhibited the phosphorylation of Raf-1, MEK1/2, and ERK1/2, while this regulation effect was abrogated by miR-195-5p inhibitor. Conclusion: LINC00662 regulated the proliferation, apoptosis, migration, and invasion of BC cells probably via miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK signaling pathway.

In this study, we aim at investigating the expression and regulation role of long non-coding RNA (lncRNA) DLX6-AS1 in bladder cancer (BC). DLX6-AS1 was highly expressed in BC tissues and significant negative correlation with the 5-year survival in the BC patients. The results showed that the proliferation, migration and invasion activities of BC cells were promoted by DLX6-AS1 overexpression, while cell apoptosis was repressed. However, knockdown DLX6-AS1 presented an pposite regulatory effect, and DLX6-AS1 knockdown delayed tumor in vivo. The potential target of DLX6-AS1 in BC was predicted and verified by RIP, RNA pull-down, and dual-luciferase reporter assays as miR-195-5p. The results showed that miR-195-5p was down-regulated in BC tissues, the expression of which was significantly negative correlated with DLX6-AS1 expression. In addition, the results also showed that miR-195-5p targeted and down-regulated the VEGFA. Knockdown of DLX6-AS1 up-regulated miR-195-5p expression and down-regulated VEGFA expression. Moreover, down-regulation of VEGFA expression caused by DLX6-AS1 inhibited phosphorylation of Raf-1, MEK1/2, and ERK1/2, while miR-195-5p inhibitors abolished the effect of silencing DLX6-AS1 expression. Our study demonstrated that DLX6-AS1 played an oncogenic role in BC through miR-195-5p-mediated VEGFA/Ras/Raf/MEK/ERK pathway.

Bladder cancer (BCa) is a common urinary tract malignancy with frequent recurrences after initial resection. Submucosal injection of gemcitabine prior to transurethral resection of bladder tumor (TURBT) may prevent recurrence of urothelial cancer. However, the underlying mechanism remains unknown. In the present study, ultra-performance liquid chromatography Q-Exactive mass spectrometry was used to profile tissue metabolites from 12 BCa patients. The 48 samples included pre- and post-gemcitabine treatment BCa tissues, as well as adjacent normal tissues. Principal component analysis (PCA) revealed that the metabolic profiles of pre-gemcitabine BCa tissues differed significantly from those of pre-gemcitabine normal tissues. A total of 34 significantly altered metabolites were further analyzed. Pathway analysis using MetaboAnalyst identified three metabolic pathways closely associated with BCa, including glutathione, purine and thiamine metabolism, while gluta-thione metabolism was also identified by the enrichment analysis using MetaboAnalyst. In search of the possible targets of gemcitabine, metabolite profiles were compared between the pre-gemcitabine normal and post-gemcitabine BCa tissues. Among the 34 metabolites associated with BCa, the levels of bilirubin and retinal recovered in BCa tissues treated with gemcitabine. When comparing normal bladder tissues with and without gemcitabine treatment, among the 34 metabolites associated with BCa, it was observed that histamine change may be associated with the prevention of relapse, whereas thiamine change may be involved in possible side effects. Therefore, by employing a hypothesis-free tissue-based metabolomics study, the present study investigated the metabolic signatures of BCa and found that bilirubin and retinal may be involved in the mechanism underlying the biomolecular action of submucosal injection of gemcitabine in urothelial BCa.

In cognitive radio, most of existing research efforts devoted to spectrum sharing have two weakness as follows. First, they are largely formulated as a Markov decision process (MDP), which requires a complete knowledge of channel. Second, most of the studies are online learning based on perceived channel. To solve the above problems, a new algorithm is proposed in this paper: if the authorized user exists in the current channel, Second user will send conservatively in low rate, or send aggressively. When sending conservatively, the state of the channel is not directly observable, the problem turns out to be Partially Observable Markov Decision Process (POMDP).We first establish the optimal threshold when the channel is known, then consider the optimal transmission when the channel is unknown and model for multi-armed bandit. We get the optimal K-conservative policy through the UCB algorithm and improve the convergence speed by UCB-TUNED algorithm. Simulation and analysis results show that it is the same result of K-conservative policy no matter the multiarmed bandit online learning under not fully known channel or the optimal threshold policy under known channel .At the same time, we improve the convergence speed by UCB-TUNED algorithm.

microRNAs (miRNAs) are non-coding RNAs which have the capacity to regulate gene expression at the post-transcriptional level, and have emerging as key factors involved in cancer at all stages ranging from initiation to metastasis. In the present review, we summmarize the diverse roles of the microRNA-29 (miR-29) family in cancer. First, we present a concise introduction to the miR-29 family and the expression profile of miR-29 in various cancer types. We next highlight the upstream regulatory pathway of miR-29 and describe the relationship between miR-29 and cancer in detail. As a tumor suppressor, miR-29 restrains cancer progression by promoting tumor cell apoptosis, by suppressing DNA methylation of tumor-suppressor genes, by reducing proliferation of tumors and by increasing chemosensitivity. However, as a tumor promoter, miR-29 mediates epithelial-mesenchymal transition (EMT) and promotes metastasis in breast cancer and colon cancer. Finally, we suggest that miR-29 represents a novel diagnostic and prognostic biomarker or a therapeutic target for cancer. Our review highlights the diverse relationship between miR-29 and cancer (particularly digestive system neoplasms). Further research of miR-29 in cancer is warranted.