Prakash S. Bisen

Biology of Cox-2: An Application in Cancer Therapeutics

Cyclooxygenase-2 (Cox-2) is an inducible enzyme involved in the conversion of arachidonic acid to prostaglandin and other eicosanoids. Molecular pathology studies have revealed that Cox-2 is over-expressed in cancer and stroma cells during tumor progression, and anti-cancer chemo-radiotherapies induce expression of Cox-2 in cancer cells. Elevated tumor Cox-2 is associated with increased angiogenesis, tumor invasion and promotion of tumor cell resistance to apoptosis. Several experimental and clinical studies have established potent anti-cancer activity of NSAID (Non-steroidal anti-inflammatory drugs) and other Cox-2 inhibitors such as celecoxib. Much attention is being focused on Cox-2 inhibitors as beneficial target for cancer chemotherapy. The mode of action of Cox-2 and its inhibitors remains unclear. Further clinical application needs to be investigated for comprehending Cox-2 biological functions and establishing it as an effective target in cancer therapy.

Biodiesel production with special emphasis on lipase-catalyzed transesterification

The production of biodiesel by transesterification employing acid or base catalyst has been industrially accepted for its high conversion and reaction rates. Downstream processing costs and environmental problems associated with biodiesel production and byproducts recovery have led to the search for alternative production methods. Recently, enzymatic transesterification involving lipases has attracted attention for biodiesel production as it produces high purity product and enables easy separation from the byproduct, glycerol. The use of immobilized lipases and immobilized whole cells may lower the overall cost, while presenting less downstream processing problems, to biodiesel production. The present review gives an overview on biodiesel production technology and analyzes the factors/methods of enzymatic approach reported in the literature and also suggests suitable method on the basis of evidence for industrial production of biodiesel.

Micropropagation: A Tool for the Production of High Quality Plant-based Medicines

Medicinal plants are the most important source of life saving drugs for the majority of the worlds population. The biotechnological tools are important to select, multiply and conserve the critical genotypes of medicinal plants. Plant tissue culture techniques offer an integrated approach for the production of standardized quality phytopharmaceutical through mass-production of consistent plant material for physiological characterization and analysis of active ingredients. Micropropagation protocols for cloning of some medicinal plants such as Catharanthus roseus (Apocynaceae), Chlorophytum borivilianum (Liliaceae), Datura metel (Solanaceae), and Bacopa monnieri (Scrophulariaceae) have been developed. Regeneration occurred via organogenesis and embryogenesis in response to auxins and cytokinins. The integrated approaches of our culture systems will provide the basis for the future development of novel, safe, effective, and high-quality products for consumers.

Jatropha curcas L., a multipurpose stress resistant plant with a potential for ethnomedicine and renewable energy.

Jatropha curcas is a stress--resistant perennial plant growing on marginal soils. This plant is widespread throughout arid and semiarid tropical regions of the world and has been used as a traditional folk medicine in many countries. J.curcas is a source of several secondary metabolites of medicinal importance. The leaf, fruits, latex and bark contain glycosides, tannins, phytosterols, flavonoids and steroidal sapogenins that exhibit wide ranging medicinal properties. The plant products exhibit anti-bacterial and anti-fungal activities. The paper highlights the ability of various metabolites present in the plant to act as therapeutic agents and plant protectants. The plant is designated as an energy plant and use of J.curcas oil as biodiesel is a promising and commercially viable alternative to diesel oil. The seeds of the plant are not only a source of biodiesel but also contain several metabolites of pharmaceutical importance. Commercial exploitation for biopharmaceuticals and bio-energy production are some of the prospective future potential of this plant. Further reclamation of wastelands and dry lands is also possible with J.curcas cultivation.

Down-regulation of survivin by oxaliplatin diminishes radioresistance of head and neck squamous carcinoma cells

BACKGROUND Oxaliplatin is integrated in treatment strategies against a variety of cancers including radiation protocols. Herein, as a new strategy we tested feasibility and rationale of oxaliplatin in combination with radiation to control proliferation of head and neck squamous cell carcinoma (HNSCC) cells and discussed survivin-related signaling and apoptosis induction. METHODS Cytotoxicity and apoptosis induced by radiation and/or oxaliplatin were examined in relation to survivin status using two HNSCC cell lines viz., Cal27 and NT8e, and one normal 293-cell line. Survivin gene knockdown by siRNA was also tested in relevance to oxaliplatin-mediated radiosensitization effects. RESULTS Survivin plays a critical role in mediating radiation-resistance in part through suppression of apoptosis via a caspase-dependent mechanism. Oxaliplatin treatment significantly decreased expression of survivin in cancer cells within 24-72 h. Apoptotic cells and caspase-3 activity were increased parallely with decrease in cell viability, if irradiated during this sensitive period. The cytotoxicity of oxaliplatin and radiation combination was greater than additive. Survivin gene knockdown experiments have demonstrated the role of survivin in radiosensitization of cancer cells mediated by oxaliplatin. CONCLUSIONS Higher expression of survivin is a critical factor for radioresistance in HNSCC cell lines. Pre-treatment of cancer cells with oxaliplatin significantly increased the radiosensitivity through induction of apoptosis by potently inhibiting survivin.

Detection of survivin and p53 in human oral cancer: Correlation with clinicopathologic findings

Survivin, an inhibitor of apoptosis, is overexpressed in cancer. It has been implicated in both prevention of apoptosis and cell cycle regulation. We investigated the distribution of antiapoptotic protein survivin in 29 oral squamous cell carcinoma (OSCC) and 16 oral premalignant lesions. It has been suggested that wild‐type p53 represses survivin expression. Therefore, we investigated the status of p53 in relation to survivin to determine the potential involvement in oral tumorigenesis.

Oncoapoptotic signaling and deregulated target genes in cancers: Special reference to oral cancer

Cancer is a class of diseases characterized by uncontrolled cell growth. The development of cancer takes place in a multi-step process during which cells acquire a series of mutations that eventually lead to unrestrained cell growth and division, inhibition of cell differentiation, and evasion of cell death. Dysregulation of oncoapoptotic genes, growth factors, receptors and their downstream signaling pathway components represent a central driving force in tumor development. The detailed studies of signal transduction pathways for mechanisms of cell growth and apoptosis have significantly advanced our understanding of human cancers, subsequently leading to more effective treatments. Oral squamous cell carcinoma represents a classic example of multi-stage carcinogenesis. It gradually evolves through transitional precursor lesions from normal epithelium to a full-blown metastatic phenotype. Genetic alterations in many genes encoding crucial proteins, which regulate cell proliferation, differentiation, survival and apoptosis, have been implicated in oral cancer. As like other solid tumors, in oral cancer these genes include the ones coding for cell cycle regulators or oncoproteins (e.g. Ras, Myc, cyclins, CDKs, and CKIs), tumor suppressors (e.g. p53 and pRb), pro-survival proteins (e.g. telomerase, growth factors or their receptors), anti-apoptotic proteins (e.g. Bcl2 family, IAPs, and NF-kB), pro-apoptotic proteins (e.g. Bax and BH-3 family, Fas, TNF-R, and caspases), and the genes encoding key transcription factors or elements for signal transduction leading to cell growth and apoptosis. Here we discuss the current knowledge of oncoapoptotic regulation in human cancers with special reference to oral cancers.

Molecular Diagnostics: Promises and Possibilities

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Prevalence of Metabolic Syndrome in Type 2 Diabetes Mellitus Using NCEP-ATPIII, IDF and WHO Definition and Its Agreement in Gwalior Chambal Region of Central India

The aim of study was to determine the prevalence of metabolic syndrome (MetS) in people with type 2 diabetes mellitus (T2DM). National Cholesterol Education Program (NCEP) ATPIII Criteria, International Diabetes Federation and the World Health Organization (WHO) definitions were used in quantifying the metabolic syndrome and also the concordance between these three criteria’s used for identifying metabolic syndrome. Methods: This cross-sectional study involved 700 type 2 diabetic subjects from the urban areas of Gwalior Chambal region (Central India). Subjects in the age group of 28-87 yrs were included in the study. Type I diabetics, pregnant ladies and those with chronic viral and bacterial infections and serious metabolic disorders were excluded from the study. Fasting blood glucose, Blood lipids (T-cholesterol, triglyceride, HDL-cholesterol) were assessed and anthropometry blood pressure were measured from all the subjects. Results: The Prevalence of metabolic syndrome was found to be 45.8%, 57.7% and 28% following NCEP-ATPIII Criteria, IDF and WHO definitions, respectively. Using all the three definitions the prevalence was higher in women in all age groups. ATP III and IDF criteria showed good agreement (κ 0.68) compared to ATP III with WHO (κ 0.54) and IDF with WHO (κ 0.34) criteria. Highest prevalence was observed following IDF definition. Conclusions: A good agreement was observed between ATPIII and IDF criteria. Maximum prevalence of Metabolic syndrome was recorded when IDF criteria was followed. NCEP-ATPIII criteria for the diagnosis of MetS and this criterion reflected equal importance to the every variable and showed a good agreement between the different criteria used.

Induction of Apoptosis and Sensitization of Head and Neck Squamous Carcinoma Cells to Cisplatin by Targeting Survivin Gene Expression

Survivin is known to be highly-expressed in various carcinomas; and is associated with their biologically aggressive characteristics and drug resistance. We have previously reported survivin as an important anti-apototic protein involved in head and neck squamous cell carcinoma (HNSCC) tumorigenesis and providing resistance to conventional cancer therapies. The purpose of present study was to investigate the potential of survivin as a therapeutic target in HNSCC. This study was designed to explore the effect(s) of survivin-siRNA therapy on the apoptosis in HNSCC cells, and its influence on cisplatin-sensitivity. Lentivirus vector was developed to deliver survivin specific siRNA into cancer cells. The data indicates that silencing of survivin-mediated by Lentivirus-siRNA therapy effectively suppressed cancer cell proliferation and induced caspase-dependent apoptosis in HNSCC cells. The study also shows that the response of HNSCC cells to cisplatin drug treatment at clinically relevant level was limited. We observed survivin to be a key factor involved in this cisplatin-resistance mechanism, and down-regulation of survivin significantly increased sensitivity of cancer cells to cisplatin-mediated apoptosis. Thus, this combination therapy acts as a multimodality regimen with significant potential to improve clinical outcomes in head and neck cancers.