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    Cycloartane-type sapogenol derivatives inhibit NF kappa B activation as chemopreventive strategy for inflammation-induced prostate carcinogenesis
    (Elsevier Science Inc, 2018) Debelec-Butuner, Bilge; Ozturk, Mert Burak; Tag, Ozgur; Akgun, Ismail Hakki; Yetik-Anacak, Gunay; Bedir, Erdal; Korkmaz, Kemal Sami
    Chronic inflammation is associated to 25% of cancer cases according to epidemiological data. Therefore, inhibition of inflammation-induced carcinogenesis can be an efficient therapeutic approach for cancer chemoprevention in drug development studies. It is also determined that anti-inflammatory drugs reduce cancer incidence. Cell culture-based in vitro screening methods are used as a fast and efficient method to investigate the biological activities of the biomolecules. In addition, saponins are molecules that are isolated from natural sources and are known to have potential for tumor inhibition. Studies on the preparation of analogues of cycloartane-type sapogenols (9,19-cyclolanostanes) have so far been limited. Therefore we have decided to direct our efforts toward the exploration of new anti-tumor agents prepared from cycloastragenol and its production artifact astragenol. The semi-synthetic derivatives were prepared mainly by oxidation, condensation, alkylation, acylation, and elimination reactions. After preliminary studies, five sapogenol analogues, two of which were new compounds (2 and 3), were selected and screened for their inhibitory activity on cell viability and NF kappa B signaling pathway activity in LNCaP prostate cancer cells. We found that the astragenol derivatives 1 and 2 as well as cycloastragenol derivatives 3, 4, and 5 exhibited strong inhibitory activity on NF kappa B signaling leading the repression of NF kappa B transcriptional activation and suppressed cell proliferation. The results suggested that these molecules might have significant potential for chemoprevention of prostate carcinogenesis induced by inflammatory NF kappa B signaling pathway.
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    Use of Non-steroidal Anti-inflammatory Drugs for Chemoprevention of Inflammation-induced Prostate Cancer
    (Turkish Pharmacists Assoc, 2017) Debelec Butuner, Bilge; Ozturk, Mert Burak
    Objectives: Chronic inflammation has been known as one of the major causes of cancer progression and 25% of cancer cases initiate due to chronic inflammation according to epidemiologic data. It has been determined that chronic inflammation induces carcinogenesis through the abrogation of cell proliferation, apoptosis, and angiogenesis mechanisms. Therefore, it is believed that inhibition of inflammation-induced carcinogenic mechanisms is an efficient therapeutic strategy in drug development studies of cancer chemoprevention. It has also been observed that use of anti-inflammatory drugs reduces the incidence of cancer, and the risk of developing prostate cancer decreases 15-20% with regular use of aspirin and non-steroidal anti-inflammatory drugs (NSAID). Materials and Methods: In this study, we investigated the effects of some clinically used NSAIDs on cellular mechanisms that play a role in inflammation-induced prostate carcinogenesis. Inhibition activities on the nuclear factor kappa-B signaling pathway, which activates tumorigenic mechanisms, as well as alterations on androgen receptor signaling, which regulates the proliferation of prostate cells, were investigated. In addition, protein kinase B (Akt) activation, which is stimulated a the inflammatory microenvironment, was examined. Results: The results showed that anti-inflammatory agents alter the protein levels of androgen receptors as well as tumor suppressor NKX3.1, and might trigger an unexpected increase in Akt((S473)) level, which induces tumorigenesis. Conclusion: It is suggested that inflammatory pathways and prostate carcinogenesis-specific mechanisms should be taken into account for the use of anti-inflammatory drugs for chemoprevention of inflammation-induced prostate cancer.