Carl zeiss zen lite software co-localization intensity
Interaction of LANA with glycogen synthase kinase (GSK)-3β, leads LANA-induced β-catenin stabilization, which is mediated by the The authors previously reported that KSHV Maintain the malignant phenotype and to ensure PEL cell survival,Ĭell cycle progression, apoptosis inhibition and immune escape Wnt/β-catenin, AKT, p53, Jak/STAT and interferon signaling to Several lytic phase-related molecules, dysregulate nuclearįactor-κB (NF-κB), mitogen-activated protein kinases (MAPKs), Latency-associated nuclear antigen (LANA)/ORF73, kaposin/K12, viral KSHV establishes a latent infection in PELĬells and expresses several viral molecules, including viralįLIP/open reading frame (ORF)71, viral cyclin/ORF72, Genome circularizes to form a double-stranded episome in the KSHV is the causative agent of Kaposi's sarcoma, PEL and Herpesvirus-8 (HHV-8)] and often with Epstein-Barr virus (EBV). Sarcoma-associated herpesvirus [KSHV, also known as human Who have undergone organ transplantation and are prescribed Patients with acquired immunodeficiency syndrome (AIDS) or those Lymphoma that develops in immunocompromised individuals, such as in Primary effusion lymphoma (PEL), also referred to asīody cavity-based lymphoma, is classified as a non-Hodgkin's B cell Thus, derivative #5 may be utilized as a novel therapeutic agent for the treatment of PEL. On the whole, these findings provide evidence that the pyridinium‑type fullerene derivative #5 exhibits antitumor activity against PEL cells in vitro and in vivo. Furthermore, the administration of derivative #5 suppressed the development of PEL cells in the ascites of SCID mice with tumor xenografts derived from PEL cells. Thus, derivative #5 overcame LANA‑mediated β‑catenin stabilization. The data demonstrated that derivative #5 increased β‑catenin phosphorylation, which resulted in β‑catenin polyubiquitination and subsequent degradation.
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The Wnt/β‑catenin activation in KSHV‑infected cells is mediated by KSHV latency‑associated nuclear antigen (LANA). It is known that the constitutive activation of Wnt/β‑catenin signaling is essential for the growth of KSHV‑infected cells. Furthermore, derivative #5 induced the destabilization of β‑catenin and suppressed β‑catenin‑TCF4 transcriptional activity in PEL cells. Derivative #5 suppressed the viability of KSHV‑infected PEL cells compared with KSHV‑uninfected B‑lymphoma cells. This analysis revealed a pyridinium‑type derivative (derivative #5 3‑5'‑(etho xycarbonyl)‑1',5'‑dihydro‑2'H‑fullereno‑C 60‑I h‑pyrrol‑2'‑yl]‑1‑methylpyridinium iodide), which exhibited antitumor activity against PEL cells via the downregulation of Wnt/β‑catenin signaling. In the present study, the growth inhibitory effects of pyrrolidinium‑type (derivatives #1 and #2), pyridinium‑type (derivatives #3 and #5 to #9) and anilinium‑type fullerene derivatives (derivative #4) against PEL cells were evaluated. In order to discover potential novel anti‑tumor compounds against PEL, the authors previously developed a pyrrolidinium‑type fullerene derivative, 1,1,1',1'‑tetramethyl fullerenodipyrrolidinium diiodide (derivative #1), which induced the apoptosis of PEL cells via caspase‑9 activation. Therefore, the discovery of novel drug candidates for the treatment of PEL is of utmost importance. PEL is an aggressive type of lymphoma and is frequently resistant to conventional chemotherapeutics. Primary effusion lymphoma (PEL) is defined as a rare subtype of non‑Hodgkin's B cell lymphoma, which is caused by Kaposi's sarcoma‑associated herpesvirus (KSHV) in immunosuppressed patients.