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MicroRNAs (miRNAs) play an important role in cancers. A number of miRNA expression-profiling studies have been done to identify the miRNA signatures of cancers from different cellular origin. There is, however, relatively little information on how anticancer agents regulate miRNA expression. Ellagitannin (BJA3121), 1,3-Di-O-galloyl-4,6-(s)-HHDP-b-D-glucopyranose, is a new natural polyphenol compound isolated from Balanophora Japonica MAKINO. Our preliminary results have shown that BJA3121 had antiproliferative effect and modified the expression of different genes in human HepG(2) cancer cells. In this study, we further evaluate whether this antineoplastic compound is able to alter miRNA expression in HepG(2) cells. We demonstrated for the first time that BJA3121 can regulate the expression of 25 miRNAs, including 17 upregulated and 8 downregulated miRNAs in HepG(2) cells. Our results suggested that BJA3121-modifed miRNA expression can mediate, at least in part, the antiproliferative and multigene regulatory action induced by the compound on HepG(2) cancer cells.

Ovarian cancer is a gynecological malignancy with high mortality rates worldwide and novel diagnostic and prognostic markers and therapeutic targets are urgently required. The suppressor of cytokine signaling 1 (SOCS1) and cyclin-dependent kinase inhibitor 1A (p21KIP) are known to regulate tumor cell proliferation. However, the mechanisms that regulate these genes have not yet been completely elucidated. In the present study, analysis of a published microarray-based high-throughput assessment (NCBI/E-MTAB-1067) and real-time PCR demonstrated that miR-572 was upregulated in human ovarian cancer tissues and cell lines. Kaplan-Meir analysis indicated that high level expression of miR-572 was associated with poorer overall survival. Ectopic miR-572 promoted ovarian cancer cell proliferation and cell cycle progression in vitro and tumorigenicity in vivo. SOCS1 and p21 were identified as direct targets of miR-572 and suppression of SOCS1 or p21 reversed the inhibiting-function of miR-572-silenced cell on proliferation and tumorigenicity in ovarian cancer cells. Additionally, the expression of miR-572 correlated inversely with the protein expression levels of SOCS1, p21 and positively with Cyclin D1 in ovarian carcinoma specimens. This study demonstrates that miR-572 post-transcriptionally regulates SOCS1 and p21 and may play an important role in ovarian cancer progression; miR-572 may represent a potential therapeutic target for ovarian cancer therapy.

The reduction of NO* with NH3 on a series of alumina-supported iron oxide-chromium oxide catalysts has been studied in flow reactors using simulated flue gas temperatures from 200 to 500 °C. The optimum catalyst contained 10 wt % of the active metal oxides at a weight ratio of 9/1 Fe:Cr. Conversion of NO*, which maximized at 400 °C, was not affected by the presence of C02 or H20 but was sharply increased with increase in oxygen between 0 and 0.5%; between 0.5 and 5.0% 02, however, NO* conversion did not undergo as substantial a relative increase with increase in oxygen concentration. Continuous operation of the flow reactor for over 1000 h showed that the 10% Fe-Cr (9/1) catalyst was effective for the selective removal of NO* (1000 ppm nominal concentration) with NH3 in simulated flue gas containing up to 1500 ppm of SO*. An intrinsic rate expression was developed for design use between 250 and 450 °C, up to 1500 ppm of NO, NH3/NO ratios of 0.5 to 3.0, and 0.5 to 5% 02.Literature Cited

Vanadium pentoxide-alumina catalysts have been shown to be both highly effective for the selective removal of NO* with NH3 in simulated flue gas and resistant to SO* during an exposure period of over 600 h. During the durability test, the nominal inlet concentrations were about 1000 ppm of NO*, 0.5 to 1.5 mole ratio of NH3/NO, and up to 2500 ppm of SO*. Although variations in H20 and C02 in the concentration ranges applicable to power plant exhausts did not affect catalytic activity, the excess oxygen greatly enhanced NO* removal. This acceleration effect was most pronounced with increase in 02 concentration below 0.5% 02. The intrinsic rate expression developed for NO* removal over the 15% V205-Al203 catalyst indicates strong pore diffusion effects between 200 and 400 °C.

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Antitumor immune responses are mediated primarily by T cells. Downregulation of the major histocompatibility complex (MHC) and the molecules that costimulate the immune response is associated with defective signaling by tumor cells for T-cell activation. In vitro treatment with a combination of cytokines significantly increased the expression of MHC class I and adhesion molecules on tumor cell surfaces. When tumor cells were first incubated with a bispecific monoclonal antibody that binds antigen on tumor cells to CD28 on T cells, the modified tumor cells become immunogenic and are able to stimulate naive T cells, generating tumor-specific cytotoxic T cells in vitro. Immunization with the modified tumor cells elicits an immune response mediated by CD8+ T cells. This response protected against a challenge with parental tumor cells and cured established tumors. The approach was effective in both low immunogenic and nonimmunogenic tumor model systems. Modification of tumor cells with this two-step procedure may provide a strategy for development of tumor vaccines that is effective for cancer immunotherapy.

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