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Tissue C1q, compared to age-matched normal prostate tissues.Ĭonclusions/Significance:We conclude that complement C1q may induce apoptosis of prostate cancer cells by activating Remarkably, as determinedīy immunostaining, benign prostatic hyperplasia and prostate cancer were shown to have a significantly reduced expression of These cells then underwent shrinkage, membrane blebbing and death. By total internal reflection fluorescence (TIRF) microscopy, it was determined that C1q destabilizedĪdherence of WOX1-expressing DU145 cells by partial detaching and inducing formation of clustered microvilli for focal adhesion A dominant negative and Y33R mutant of WOX1 blocked the apoptotic effect. Notably, exogenous C1q significantly induced apoptosis of WOX1-overexpressing DU145 cells, but not Under C6-free conditions, HA induced activation of STAT3, an enhancer of Without serum complement C9, p53 becameĪctivated, and hyaluronan (HA) reversed the effect. Rapidly restored the WOX1 activation (with Tyr33 phosphorylation) in less than 2 hr. Under complement C1q- or C6-free conditions, WOX1 and ERK were mainly present in theĬytoplasm without phosphorylation, whereas phosphorylated JNK1 was greatly accumulated in the nuclei. Methodology/Principal Findings:DU145 cells were cultured overnight in 1% normal human serum, or in human serum depleted We examined specific serum complement components in coordinating theĪctivation of tumor suppressors p53 and WWOX (also named FOR or WOX1) and kinases ERK, JNK1 and STAT3 in human Republic of China,9Department of Neuroscience and Physiology, SUNY Upstate Medical University, Syracuse, New York, United States of Americaīackground:Tissue exudates contain low levels of serum complement proteins, and their regulatory effects on prostateĬancer progression are largely unknown. Tainan, Taiwan, Republic of China,8Center for Gene Regulation and Signal Transduction Research, National Cheng Kung University Medical College, Tainan, Taiwan, South Carolina, Charleston, South Carolina, United States of America,7Department of Microbiology and Immunology, National Cheng Kung University Medical College, Taiwan, Republic of China,4Institute of Molecular Medicine, National Cheng Kung University Medical College, Tainan, Taiwan, Republic of China,5Department ofĮngineering Science, National Cheng Kung University, Tainan, Taiwan, Republic of China,6Section of Oral Biology, Department of Stomatology, Medical University of University Medical College, Tainan, Taiwan, Republic of China,3Department of Anatomy and Cell Biology, National Cheng Kung University Medical College, Tainan, Boackle6, Li-Jin Hsu7,8*, Nan-Shan Chang1,4,8,9*ġGuthrie Research Institute, Laboratory of Molecular Immunology, Sayre, Pennsylvania, United States of America,2Department of Pathology, National Cheng Kung Qunying Hong1, Chun-I Sze2,3, Sing-Ru Lin4, Ming-Hui Lee4, Ruei-Yu He5, Lori Schultz1, Jean-Yun Chang4,
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Complement C1q Activates Tumor Suppressor WWOX to Induce Apoptosis in Prostate Cancer Cells