The long, noncoding RNA (lncRNA) is an important epigenetic regulator with a critical role in human tumors. Here, we aimed to investigate the clinical application and the potential molecular mechanisms of in gastric cancer tumorigenesis and progression. The expression level of was determined by RT-qPCR analysis in 190 pairs of gastric cancer tissues and adjacent normal gastric mucosa tissues (ANT). The biologic functions of were assessed by and functional experiments. RNA protein pull-down assays and LS/MS mass spectrometry analysis were performed to detect and identify the interacting protein FOXM1. Protein-RNA immunoprecipitation assays were conducted to examine the interaction of FOXM1 and Chromatin immunoprecipitation (ChIP) and luciferase analyses were utilized to identify the binding site of FOXM1 on the promoter. The lncRNA was significantly upregulated in gastric cancer tissues compared with ANTs. High expression of predicted poor prognosis in patients with gastric cancer. enhanced gastric cancer cell proliferation and invasion and directly bound FOXM1 protein and increased FOXM1 posttranslationally. Moreover, is also a FOXM1-responsive lncRNA, and FOXM1 directly binds to the promoter to activate its transcription. Finally, fulfilled its oncogenic functions in a FOXM1-mediated manner. Our study suggests that promotes tumor progression by interacting with FOXM1. may be a valuable prognostic predictor for gastric cancer, and the positive feedback loop of -FOXM1 could be a therapeutic target in pharmacologic strategies..

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Background: MicroRNAs are important for colorectal cancer signal transduction. Results: miR-31 stimulates colorectal cancer cell proliferation and tumorigenesis by directly targeting RASA1. Conclusion: miR-31 activates the RAS pathway and functions as an oncogenic microRNA in human colorectal cancer. Significance: Learning how miRNAs participate in tumor signaling is crucial for understanding tumor signal transduction and cancer therapy.

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The widespread distribution of cyanobacteria in the aquatic environment is increasing the risk of water pollution caused by cyanotoxins, which poses a serious threat to human health. However, the structural characterization, distribution and identification techniques of cyanotoxins have not been comprehensively reviewed in previous studies. This paper aims to elaborate the existing information systematically on the diversity of cyanotoxins to identify valuable research avenues. According to the chemical structure, cyanotoxins are mainly classified into cyclic peptides, alkaloids, lipopeptides, nonprotein amino acids and lipoglycans. In terms of global distribution, the amount of cyanotoxins are unbalanced in different areas. The diversity of cyanotoxins is more obviously found in many developed countries than that in undeveloped countries. Moreover, the threat of cyanotoxins has promoted the development of identification and detection technology. Many emerging methods have been developed to detect cyanotoxins in the environment. This communication provides a comprehensive review of the diversity of cyanotoxins, and the detection and identification technology was discussed. This detailed information will be a valuable resource for identifying the various types of cyanotoxins which threaten the environment of different areas. The ability to accurately identify specific cyanotoxins is an obvious and essential aspect of cyanobacterial research.

Pseudogenes play a crucial role in cancer progression. However, the role of pituitary tumour‐transforming 3, pseudogene (PTTG3P) in gastric cancer (GC) remains unknown. Here, we showed that PTTG3P expression was abnormally up‐regulated in GC tissues compared with that in normal tissues both in our 198 cases of clinical samples and the cohort from The Cancer Genome Atlas (TCGA) database. High PTTG3P expression was correlated with increased tumour size and enhanced tumour invasiveness and served as an independent negative prognostic predictor. Moreover, up‐regulation of PTTG3P in GC cells stimulated cell proliferation, migration and invasion both in vitro in cell experiments and in vivo in nude mouse models, and the pseudogene functioned independently of its parent genes. Overall, these results reveal that PTTG3P is a novel prognostic biomarker with independent oncogenic functions in GC.

Retinoic acid (RA) is a major chemopreventive agent which exerts strong anti-tumor activity partly by trans-repressing the Wnt/beta-catenin signaling pathway in some tumor cell lines. However, the definite mechanism of RA trans-repression of the Wnt/beta-catenin signaling pathway has not been elucidated clearly. In this work, we found that all-trans retinoic acid (ATRA) significantly inhibited proliferation of glioma cells, accompanied by up-regulation of expression of Axin and altered subcellular distribution of beta-catenin. Transfecting C6 cells with rAxin further confirmed that increased expression of Axin is obligate for inhibition of proliferation and the increase of the cytoplasmic beta-catenin. Our results suggested that Axin might play an important role in RA-mediated anti-proliferative effects of glioma cell lines.

Gastric cancer (GC) is one of the most common malignancies of the digestive system worldwide. Multiple long noncoding RNAs (lncRNAs) participate in the regulation of GC development and metastasis. In this study, we aimed to elucidate the expression and function of lncRNA IGFL2‐AS1 in GC. We found that IGFL2‐AS1 was highly expressed in GC tissues and cell lines. Knockdown of IGFL2‐AS1 suppressed GC cell proliferation, migration, and invasion in vitro. Furthermore, we identified that IGFL2‐AS1 exerted its function as a molecular sponge of miR‐802. MiR‐802 was demonstrated to be a tumor suppressor, and overexpression of miR‐802 suppressed GC cell growth, migration, and invasion. Mechanistically, we revealed that the cAMP‐regulated phosphoprotein 19 (ARPP19) was a direct target of miR‐802 and could reverse the inhibitory function of miR‐802. Moreover, our results confirmed that knockdown of IGFL2‐AS1 inhibited GC tumor development in an in vivo GC tumor xenograft model. In summary, our data suggest that the IGFL2‐AS1/miR‐802/ARPP19 axis plays a critical role in the progression and metastasis of GC. Therapies targeting the IGFL2‐AS1/miR‐802/ARPP19 axis can potentially improve GC treatment.