Naturally-occurring chalcones and synthetic chalcone analogues have been demonstrated to have many biological effects, including anti-inflammatory, anti-malarial, anti-fungal, and anti-oxidant/anti-cancerous activities. Compared to other chalcones, trans-chalcone exhibits superior inhibitory activity in cancer cell growth as shown via in vitro assays, and exerts anti-cancerous effects via the activation of the p53 tumor suppressor protein. Thus, characterization of the specific mechanisms, by which trans-chalcone activates p53, can aid development of new chemotherapeutic drugs that can be used individually or synergistically with other drugs. In this report, we found that trans-chalcone modulates many p53 target genes, HSP40 being the most induced gene in the RNA-Seq data using trans-chalcone-treated cells. CRM1 is also inhibited by trans-chalcone, resulting in the accumulation of p53 and other tumor suppressor proteins in the nucleus. Similar effects were seen using trans-chalcone derivatives. Overall, trans-chalcone could provide a strong foundation for the development of chalcone-based anti-cancer drugs.
Background/Aim: Plasma medicine is a new field that provides great potential for the treatment of human diseases including cancer in addition to sterilizing the surface of skin and facilitating wound healing. Recently, nonthermal atmospheric plasma (or cold atmospheric plasma, CAP) was introduced, not only for denaturing cells and tissues, but also for operating under the threshold of thermal damage and for chemically inducing a specific response or modification. Materials and Methods: Microwave-mediated CAP was used in this study. Results: CAP increased highmobility group box 1 protein (HMGB1) expression, thereby increasing HMGB-1 secretion. In addition, we observed that the calreticulin (CRT) protein was concentrated at the cellular membrane when plasma was treated, representing immunogenic cell death. Conclusion: Overall, plasma treatment induces apoptosis via immunogenic cell death in cancer cells, implying a potential application to human cancer therapy and for the treatment of other human diseases.Cancer is the second leading cause of death in the USA, and conventional therapeutic approaches including chemo/radio therapy could not face the current crisis. New technologies, concepts, or combination therapies are needed to improve the current situation. Plasma is an energy that consists of active
Purpose of review Liver transplantation is the gold standard for the treatment of end-stage liver disease. However, a shortage of donor organs, high cost, and surgical complications limit the use of this treatment. Cellular therapies using hepatocytes, hematopoietic stem cells, bone marrow mononuclear cells, and mesenchymal stem cells (MSCs) are being investigated as alternative treatments to liver transplantation. The purpose of this review is to describe studies using MSC transplantation for liver diseases based on the reported literature and to discuss prospective research designed to improve the efficacy of MSC therapy. Recent findings MSCs have several properties that show potential to regenerate injured tissues or organs, such as homing, transdifferentiation, immunosuppression, and cellular protective capacity. Additionally, MSCs can be noninvasively isolated from various tissues and expanded ex vivo in sufficient numbers for clinical evaluation. Summary Currently, there is no approved MSC therapy for the treatment of liver disease. However, MSC therapy is considered a promising alternative treatment for end-stage liver diseases and is reported to improve liver function safely with no side effects. Further robust preclinical and clinical studies will be needed to improve the therapeutic efficacy of MSC transplantation.
PGE 2 is the major lipid mediator of inflammation produced by multiple cell types including follicular dendritic cells (FDCs) of the lymphoid tissue. We have investigated the immunoregulatory function of PGE 2 and its production mechanism using FDC-like cells isolated from human tonsil. Our recent observation of COX-2-inducing effect of PGE 2 prompted us to identify the responsible receptor in this study. Pharmacologic approaches were adopted and Western blotting was utilized to measure protein expression levels. Agonists selective for EP2 and EP4 significantly stimulated COX-2 expression, while antagonists for these receptors prevented PGE 2 from triggering COX-2 induction. The combined addition of EP2 and EP4 antagonists resulted in further inhibition of PGE 2. In contrast, EP1 and EP3 antagonists failed to exhibit the inhibitory effect on PGE 2-induced COX-2 expression. Since PGE 2 achieves COX-2 induction by repressing Akt activation in FDC-like cells, we confirmed EP2 and EP4 being the targets of PGE 2 by examining the effects of E-prostanoid (EP) agonists and antagonists on the level of Akt phosphorylation. After the identification of PGE 2 receptor, we examined the effect of PGE 2 on IL-1β-induced COX-2 expression. PGE 2 and IL-1β brought about a synergistic induction of COX-2 expression. Taken together, this study implies the impact of the combined role of eicosanoids and cytokines in inflammatory milieu.
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