Lupeol (Lup-20(29)-en-3H-ol), a novel dietary triterpene, was found in fruits, vegetables, and several medicinal plants. Here, we investigated its growth-inhibitory effect and associated mechanisms in hepatocellular carcinoma SMMC7721 cells. Lupeol treatment resulted in significant inhibition of cell viability in a dose-dependent manner and caused apoptotic death of this cell line with activation of caspase3 expression. Caspase8 inhibitor pretreatment was found to partially block the apoptosis induced by Lupeol. Moreover, Lupeol specifically caused a significant decrease in the expression of Death receptor 3 (DR3) mRNA and protein and a significant elevated expression of FADD mRNA whereas Fas mRNA and protein expression was not detectable. Further more, knockdown of DR3 by small interfering RNA inhibited the growth and induced apoptosis of hepatocellular carcinoma cell. These results suggested that Lupeol treatment induced growth inhibition and apoptosis in SMMC7721 cells, the mechanism is due to down-regulation of DR3 expression. We demonstrated that Lupeol appears to be a promising chemopreventive agent for treating hepatocellular carcinoma, and DR3 may be an important target for liver cancer therapy.

BackgroundGlioma is a common primary brain tumor with extremely poor prognosis outcomes. Increasing evidences have proved the relation between lncRNAs and glioma onset and progression. LncRNA SNHG5 involves in the biological activities of tumor cells, such as proliferation, migration and metastasis. Nevertheless, it is still necessary to explain the molecular mechanism and biofunction of SNHG5 in glioma.Materials and methodsQuantitative real-time PCR (qRT-PCR) was performed to analyze expressions of SNHG5, miR-205-5p and ZEB2 in tumor tissues and cell lines. The cell counting kit-8 (CCK-8) assay, plate and soft agar colony formation assays were performed to evaluate cell proliferation ability. RNA immunoprecipitation assay and dual-luciferase reporter assay were used to confirm the interaction among SNHG5, miR-205-5p and ZEB2. The protein level of ZEB2 was measured by Western blot.ResultsBased on our findings, compared with normal tissues, the elevated expression of SNHG5 and decreased expression of miR-205-5p were observed in glioma tissues. The downregulation of SNHG5 exerted an obvious inhibitory effect on glioma cells in terms of their proliferation. With regard to the underlying mechanism, SNHG5 presented a direct inhibitory influence on miR-205-5p which targeted to the 3′-UTR region of zinc finger E-box binding homeobox 2 (ZEB2) mRNA. As a competing endogenous RNA (ceRNA), SNHG5 sponged miR-205-5p, regulating the expression of ZEB2 thereby.ConclusionThese discoveries indicate that SNHG5 promotes proliferation of glioma by regulating miR-205-5p/ZEB2 axis.

Glioma is the most common type of primary brain cancer in adults. Accumulating studies have reported that long non-coding RNAs (lncRNAs) serve a significant role in the initiation and development of glioma. lncRNA small nucleolar RNA host gene 7 (SNHG7) has been previously demonstrated to serve a role in numerous glioma biological processes, including cell proliferation, invasion and migration. The present study aimed to investigate the role of SNHG7 in glioma through reverse transcription-quantitative PCR, western blotting and cell function assays. The results revealed that SNHG7 expression was upregulated in glioma tissues and cell lines, while microRNA (miR)-138-5p expression was downregulated. Moreover, the knockdown of SNHG7 expression decreased the proliferation of glioma cells. Mechanistic studies demonstrated that SNHG7 downregulated miR-138-5p expression, which subsequently affected the expression levels of its target gene, enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2). In conclusion, the results of the present study suggested that SNHG7 may act as a competing endogenous RNA to sponge miR-138-5p and modulate EZH2 expression. Thus, SNHG7 may enhance glioma proliferation via modulating the miR-138-5p/EZH2 signaling axis.

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The specific source of ancient sedimentary manganese (Mn) deposits is commonly complex. Here we use systematic major and trace element data with strontium (Sr) and neodymium (Nd) isotopic analyses of the Ortokarnash Mn(II) carbonate ores and associated carbonate rocks from the Upper Carboniferous Kalaatehe Formation (ca. 320 Ma) in order to constrain the Mn source. This formation consists of three members: the first member is a volcanic breccia limestone, the second member is a sandy limestone, and the third member is a black marlstone with the Mn(II) carbonate interlayers. Petrographic observations in combination with low Al2O3 (<3.0 wt%) and Hf (<0.40 ppm) contents and the lack of correlations between the Al2O3 and 87Sr/86Sr ratios as well as εNd(t) values demonstrate a negligible influence of terrigenous detrital contamination on both Sr and Nd isotopic compositions of the Mn(II) carbonate ores. The Sr isotopes of Mn(II) carbonate ores are most likely affected by post-depositional alteration, while Nd isotopes remain unaltered. The initial 87Sr/86Sr ratios in the associated carbonate rocks are likely the result of a mixture of the chemical components (i.e., seawater) and the Al-rich components (e.g., volcanoclastic material), while the detrital effects on Nd isotopes are negligible. In addition, both Sr and Nd isotopes in these non-mineralized wall rocks remained unchanged during post-depositional processes. The relatively low Th/Sc ratios and positive εNd(t) values suggest that the aluminosilicate fraction in the calcarenite and sandy limestone was mainly derived from the weathering of a depleted mafic source, representing the riverine input into the seawater. Given that the Mn(II) carbonate ores are characterized by negative εNd(t) values, these suggest that seafloor-vented hydrothermal fluids derived from interaction with the underlying old continental crust mainly contribute to the source of the Mn(II) carbonates.