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Background/Aims: Hepatocellular carcinoma (HCC) has a high morbidity as well as mortality and is believed to be one of the most prevalent cancers worldwide. The long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in numerous cancers, including HCC. This study aimed to explore the role of MALAT1 in HCC progression. Methods: The expression levels of MALAT1 and Vimentin in HCC tissues and relative pair-matched adjacent normal liver tissues were analyzed by RT-PCR, and immunohistochemistry. Using bioinformatics analysis and dual-luciferase assay, we examined the correlation between MALAT1 and miR-30a-5p. Dual-luciferase assay and western blotting suggested that Vimentin was a target of miR-30a-5p. A wound healing assay and transwell assays were employed to determine the effect of MALAT1 and miR-30a-5p on cell migration and invasion in HCC. Results: Our data demonstrated that the levels of MALAT1 and Vimentin were upregulated in HCC tissues and that miR-30a-5p was a direct target of MALAT1. Silenced MALAT1 and overexpressed miR-30a-5p each inhibited cell migration and invasion. Additionally, dual-luciferase assay and western blotting demonstrated that MALAT1 could competitively sponge miR-30a-5p and thereby regulate Vimentin. Conclusion: Our data suggest that MALAT1 acts as an oncogenic lncRNA that promotes HCC migration and invasion. Therefore, the MALAT1-miR-30a-5p-Vimentin axis is a potential therapeutic target and molecular biomarker in HCC.

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Background: PB2 cap is critical for the initiation of influenza virus transcription. Results: FluB PB2 cap binds to GDP and m 7 GDP utilizing unique structural features, which is corroborated by data from ITC. Conclusion: FluB PB2 cap has a unique cap recognition mechanism compared with FluA PB2 cap . Significance: We characterize the cap recognition mechanism of FluB PB2 cap , consequently providing insight into inhibitor design targeting FluB PB2 cap .

BackgroundAs an oncogene, long noncoding RNA metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1) can promote tumor metastasis. Hyperexpression of MALAT1 has been observed in many malignant tumors, including hepatocellular carcinoma (HCC). However, the role and mechanism of MALAT1 in HCC remain unclear.MethodsThirty human HCC and paracancerous tissue specimens were collected, and the human hepatoma cell lines Huh7 and HepG2 were cultured according to standard methods. MALAT1 and Snail family zinc finger (Slug) expression were measured by real‐time PCR, immunohistochemistry, and western blotting. Luciferase reporter assay and RNA immunoprecipitation (RIP) assay verified the direct interaction between miR‐124‐3p and Slug(SNAI2) or MALAT1. Wound healing and transwell assays were performed to examine invasion and migration, and a subcutaneous tumor model was established to measure tumor progression in vivo.ResultsMALAT1 expression was upregulated in HCC tissues and positively correlated with Slug expression. MALAT1 and miR‐124‐3p bind directly and reversibly to each other. MALAT1 silencing inhibited cell migration and invasion. miR‐124‐3p inhibited HCC metastasis by targeting Slug.ConclusionsMALAT1 regulates Slug through miR‐124‐3p, affecting HCC cell metastasis. Thus, the MALAT1/miR‐124‐3p/Slug axis plays an important role in HCC.

In arid zones, precipitation distribution is extremely uneven, with saline‐waterlogging and dry–moist cycles appearing frequently, which negatively impact on seed germination and seedling establishment. The responses of two halophytes, Suaeda physophora and Haloxylon ammodendron, and a xerophyte, Haloxylon persicum, to saline‐waterlogging and dry–moist cycles were studied. The results showed that aeration increased seed germination for all species when seeds were submerged in NaCl, especially for xerophyte. Compared with S. physophora and H. ammodendron, seed germination, recovery germination, and total germination of H. persicum were much lower when seeds were submerged in 700 mm NaCl, especially for the recovery germination and total germination of nongerminated seeds when the seeds were desiccated and then transferred to distilled water. However, when the seeds were submerged in 700 mm NaCl with aeration, the seed germination, recovery germination, and total germination of nongerminated seeds transferred to distilled water increased dramatically for H. persicum. No adverse effect of desiccation was found on those values of nongerminated seeds pretreated in NaCl with or without aeration for the two halophytes. In conclusion, seeds of the two halophytes were more tolerant to waterlogging and dry–moist cycles than seeds of the xerophyte during emergence under saline conditions; these traits may be important for halophytes to survive extreme saline environments during the seed germination stage.

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EMT (epithelial-mesenchymal transition) occurs in a wide range of tumor types, and has been shown to be crucial for metastasis. Epigenetic modifications of histones contribute to chromatin structure and result in the alterations in gene expression. Tri-methylation of histone H3 lysine 4 (H3K4me3) is associated with the promoters of actively transcribed genes and can serve as a transcriptional on/off switch. RbBP5 is a component of the COMPASS/ -like complex, which catalyzes H3K4me3 formation. In this study, we found that in the process of TGF-Beta1 induced EMT in the prostate cancer cell line DU145, H3K4me3 enrichment and RbBP5 binding increased in the vicinity of Snail (SNAI1) transcription start site. Knocking-down of RbBP5 notably decreased Snail expression and EMT. Recruitment of RbBP5 and formation of H3K4me3 at Snail TSS during EMT depend on binding of SMAD2/3 and CBP at Snail TSS. This study links the SMAD2/3 signal with Snail transcription via a histone modification - H3K4me3. Furthermore, our research also demonstrates that RbBP5 and even WRAD may be a promising therapeutic candidates in treating prostate cancer metastasis, and that DU145 cells maintain their incomplete mesenchymal state in an auto/paracrine manner.