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Microbial inulinases are an important class of industrial enzymes that have gained much attention recently. Inulinases can be produced by a host of microorganisms, including fungi, yeast, and bacteria. Among them, however, Aspergillus sp. (filamentous fungus) and Kluyveromyces sp. (diploid yeast) are apparently the preferred choices for commercial applications. Among various substrates (carbon source) employed for their production, inulin-containing plant materials offer advantages in comparison to pure substrates. Although submerged fermentation has been universally used as the technique of fermentation, attempts are being made to develop solid-state fermentation technology also. Inulinases catalyze the hydrolysis of inulin to D-fructose (fructose syrup), which has gained an important place in human diets today. In addition, inulinases are finding other newer applications. This article reviews more recent developments, especially those made in the past decade, on microbial inulinases--its production using various microorganisms and substrates. It also describes the characteristics of various forms of inulinases produced as well as their applications.

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Purpose Melanoma is a solid tumor that is notoriously resistant to chemotherapy, and its incidence is rapidly increasing. Recently, several signaling pathways have been demonstrated to contribute to melanoma tumorigenesis, including constitutive activation of MAP kinase, Akt and Stat-3. The activation of multiple pathways may account in part for the difficulty in treatment of melanoma. In a recent screen of compounds, we found that an organopalladium compound, tris (dibenzylideneacetone) dipalladium (Tris DBA), demonstrated significant antiproliferative activity against melanoma cells. Studies were carried out to determine the mechanism of action of Tris DBA Experimental Design Tris DBA was tested on efficacy on proliferation of human and murine melanoma cells. In order to find the mechanism of action of Tris DBA, we performed Western Blot analysis and gene array analysis. The ability of Tris DBA to block tumor growth in vivo was assessed. Results (Tris DBA), has activity against B16 murine and A375 human melanoma in vivo. Tris DBA inhibits several signaling pathways including activation of MAP kinase, Akt, Stat-3 and S6 kinase activation, suggesting an upstream target. Tris DBA was found to be a potent inhibitor of N-myristoyltransferase 1 (NMT-1), which is required for optimal activity of membrane based signaling molecules. Tris DBA demonstrated potent antitumor activity in vivo against melanoma. Conclusion Tris DBA is thus a novel inhibitor of NMT-1 with significant antitumor activity and is well tolerated in vivo. Further preclinical evaluation of Tris DBA and related complexes is warranted.

Colorectal cancer (CRC) is the third most common cause of cancer death in the Western world. Calcineurin (CaN), a Ca2+/calmodulin (CaM)-dependent protein phosphatase, is important for Ca2+-mediated signal transduction. The main objective of this study is to examine the potential role of Ca2+/CaM-dependent protein phosphatase in both normal and in invasive tumor components of human samples. In this study, we carried out 45 cases of CaN activity, 13 cases of CaN protein expression by Western blot analysis, and 6 cases for immunohistochemical analysis in both normal and invasive tumor components of human samples. Immunohistochemical analysis revealed that strong cytoplasmic staining of varying intensity was observed in colon tumors of all patients compared to normal mucosa. In addition, Western blot analysis revealed a prominent overexpressed immunoreactive band with an apparent molecular mass of 60 kDa catalytic alpha subunit (CaN A) as well as CaN Aalpha and beta in colon tumor samples. Elevated CaN protein expression appears to be a possible link between Ca2+ signaling and oncogenic processes.

Triple negative breast cancer (TNBC) is characterized by a lack in estrogen, progesterone, and epidermal growth factor 2 receptors. TNBC exhibits most of the characteristics of basal-like and claudin-low breast cancer subtypes. The main contributor in the mortality of TNBC is due to the higher invasive and migratory ability of these tumor cells. Some plant flavonoids inhibit the epithelial mesenchymal transition (EMT) of tumor cells and suppress cancer metastasis. In this study, we aimed to determine whether the flavonoid quercetin is effective in modulating the molecular signaling associated with EMT in TNBC. Our data indicated that quercetin can induce the expression of E-cadherin and also downregulate vimentin levels in TNBC. The ability of quercetin to modulate these EMT markers resulted in a mesenchymal-to-epithelial transition (MET). Quercetin-induced MET was linked with the alteration of nuclear localization of β-catenin and modulation of β-catenin target genes such as cyclin D1 and c-Myc. Furthermore, we observed that quercetin induced the anti-tumor activity of doxorubicin by inhibiting the migratory ability of TNBC cells. These results suggested that quercetin may inhibit TNBC metastasis and also improve the therapeutic efficacy of existing chemotherapeutic drugs.

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