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• W2137407924 abstract "Abstract Although treatment of Hodgkin's lymphoma (HL) with a multi‐drug approach has been very successful, its toxicity becomes evident after several years as secondary malignancies and cardiovascular disease. Therefore, the current goal in HL treatment is to find new therapies that specifically target the deregulated signaling cascades, such as NF‐κB and STAT3, which cause Hodgkin and Reed‐Sternberg (H‐RS) cell proliferation and resistance of apoptosis. Based on the above information, we investigated the capacity of curcumin to inhibit NF‐κB and STAT3 in H‐RS cells, characterizing the functional consequences. Curcumin is incorporated into H‐RS cells and acts inhibiting both NF‐κB and STAT3 activation, leading to a decreased expression of proteins involved in cell proliferation and apoptosis, e.g . Bcl‐2, Bcl‐xL, cFLIP, XIAP, c‐IAP1, survivin, c‐myc and cyclin D1. Interestingly, curcumin caused cell cycle arrest in G2‐M and a significant reduction (80–97%) in H‐RS cell viability. Furthermore, curcumin triggered cell death by apoptosis, as evidenced by the activation of caspase‐3 and caspase‐9, changes in nuclear morphology and phosphatidylserine translocation. The above findings provide a mechanistic rationale for the potential use of curcumin as a therapeutic agent for patients with HL. © 2008 Wiley‐Liss, Inc." @default.
• W2137407924 created "2016-06-24" @default.
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• W2137407924 date "2008-04-24" @default.
• W2137407924 modified "2023-10-18" @default.
• W2137407924 title "Curcumin induces cell‐arrest and apoptosis in association with the inhibition of constitutively active NF‐κB and STAT3 pathways in Hodgkin's lymphoma cells" @default.
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• W2137407924 doi "https://doi.org/10.1002/ijc.23477" @default.
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• W2137407924 hasPublicationYear "2008" @default.
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