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Cell Death and Differentiation

SeoYoung Kim, Hee Jin, Hang-Rhan Seo, Hae June Lee, Yun-Sil Lee
Cathepsin S (CTSS) is a cysteine protease that is thought to play a role in many physiological and pathological processes including tumor growth, angiogenesis, and metastasis; it has been identified as a radiation response gene. Here, we examined the role of CTSS in regulating the DNA damage response in breast cancer cells. Activating CTSS (producing the cleavage form of the protein) by radiation induced proteolytic degradation of BRCA1, which ultimately suppressed DNA double-strand break repair activity. Depletion of CTSS by RNAi or expression of a mutant type of CTSS enhanced the protein stability of BRCA1 by inhibiting its ubiquitination...
July 13, 2018: Cell Death and Differentiation
Layal Maatouk, Chenju Yi, Maria-Angeles Carrillo-de Sauvage, Anne-Claire Compagnion, Stéphane Hunot, Pascal Ezan, Etienne C Hirsch, Annette Koulakoff, Frank W Pfrieger, François Tronche, Luc Leybaert, Christian Giaume, Sheela Vyas
The precise contribution of astrocytes in neuroinflammatory process occurring in Parkinson's disease (PD) is not well characterized. In this study, using GRCx30CreERT2 mice that are conditionally inactivated for glucocorticoid receptor (GR) in astrocytes, we have examined the actions of astrocytic GR during dopamine neuron (DN) degeneration triggered by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The results show significantly augmented DN loss in GRCx30CreERT2 mutant mice in substantia nigra (SN) compared to controls...
July 13, 2018: Cell Death and Differentiation
Mable Lam, David A Lawrence, Avi Ashkenazi, Peter Walter
Several studies implicate specific death receptors (DRs) and caspase-8 in mediating apoptosis in response to endoplasmic reticulum (ER) stress; however, a recent paper challenges this conclusion. Here we validate the importance of DR5 and caspase-8 as critical signal conduits for apoptosis activation upon ER stress.
July 10, 2018: Cell Death and Differentiation
Polina Zjablovskaja, Miroslava Kardosova, Petr Danek, Pavla Angelisova, Touati Benoukraf, Alexander A Wurm, Tomas Kalina, Stephanie Sian, Martin Balastik, Ruud Delwel, Tomas Brdicka, Daniel G Tenen, Gerhard Behre, Fréderic Fiore, Bernard Malissen, Vaclav Horejsi, Meritxell Alberich-Jorda
Since publication of this article, the authors identified an error in the acknowledgments section. The original sentence in acknowledgments reads as follows.
July 10, 2018: Cell Death and Differentiation
Ning Zhang, Hanwen Zhang, Ying Liu, Peng Su, Jiashu Zhang, Xiaolong Wang, Mingjuan Sun, Bing Chen, Wenjing Zhao, Lijuan Wang, Huiyun Wang, Meena S Moran, Bruce G Haffty, Qifeng Yang
The progression of localized breast cancer to distant metastasis results in a poor prognosis and a high mortality rate. In this study, the contributions of miRNAs to tumor progression and the regulatory mechanisms leading to their expression alterations were investigated. Using highly lung-metastatic sub-lines from parental breast cancer cells, miRNA expression profiling revealed that the miR-17-92 cluster is significantly downregulated and the miR-18a-5p is the most evidently decreased. Ectopic expression and inhibition of miR-18a-5p demonstrated its capacity in suppressing migration and invasion of breast cancer cells...
July 9, 2018: Cell Death and Differentiation
So-Youn Kim, Devi M Nair, Megan Romero, Vanida A Serna, Anthony J Koleske, Teresa K Woodruff, Takeshi Kurita
Platinum-based chemotherapies can result in ovarian insufficiency by reducing the ovarian reserve, a reduction believed to result from apoptosis of immature oocytes via activation/phosphorylation of TAp63α by multiple kinases including CHEK2, CK1, and ABL1. Here we demonstrate that cisplatin (CDDP) induces oocyte apoptosis through a novel pathway and that temporary repression of this pathway fully preserves ovarian function in vivo. Although ABL kinase inhibitors effectively block CDDP-induced apoptosis of oocytes, oocytic ABL1, and ABL2 are dispensable for damage-induced apoptosis...
July 9, 2018: Cell Death and Differentiation
Elena Porcù, Francesca Maule, Daniele Boso, Elena Rampazzo, Vito Barbieri, Gaia Zuccolotto, Antonio Rosato, Chiara Frasson, Giampietro Viola, Allesandro Della Puppa, Giuseppe Basso, Luca Persano
Glioblastoma multiforme (GBM) is a highly vascularized and aggressive brain tumor, with a strong ability to disseminate and invade the surrounding parenchyma. In addition, a subpopulation of GBM stem cells has been reported to possess the ability to transdifferentiate into tumor-derived endothelial cells (TDECs), supporting the resistance to anti-angiogenic treatments of newly formed blood vessels. Bone Morphogenetic Protein 9 (BMP9) is critically involved in the processes of cancer cell differentiation, invasion and metastasis, representing a potential tool in order to impair the intrinsic GBM aggressiveness...
July 5, 2018: Cell Death and Differentiation
Donna Denton, Tianqi Xu, Sonia Dayan, Shannon Nicolson, Sharad Kumar
Animal development and homeostasis require the programmed removal of cells. Autophagy-dependent cell deletion is a unique form of cell death often involved in bulk degradation of tissues. In Drosophila the steroid hormone ecdysone controls developmental transitions and triggers the autophagy-dependent removal of the obsolete larval midgut. The production of ecdysone is exquisitely coordinated with signals from numerous organ systems to mediate the correct timing of such developmental programs. Here we report an unexpected role for the Drosophila bone morphogenetic protein/transforming growth factor β ligand, Decapentaplegic (Dpp), in the regulation of ecdysone-mediated midgut degradation...
June 29, 2018: Cell Death and Differentiation
Wei Han, Peishan Hu, Fan Wu, Shanshan Wang, Yan Hu, Shanshan Li, Tao Jiang, Boqin Qiang, Xiaozhong Peng
Differentiation status significantly affects the properties of malignant glioma cells, with non-stem cells inducing tumor enlargement and stem-like cells driving tumor initiation and treatment resistance. It is not completely understood how the same protein can have a distinct role in these cell populations. Here, we report that four and a half LIM domain protein 3 (FHL3) has an inhibitory effect on proliferation in non-stem glioma cells and a non-proliferative effect in glioma stem cells (GSCs). In GSCs, we show that FHL3 interacts with the Smad2/3 protein complex at the SOX4 promoter region, inhibits SOX4 transcriptional activity by recruiting PPM1A phosphatase to Smad2/3, and then suppresses GSC tumor sphere formation and self-renewal in vitro and in vivo via downregulation of SOX2 expression...
June 28, 2018: Cell Death and Differentiation
Yihong Zhang, Xiuqun Zou, Wenli Qian, Xiaoling Weng, Lin Zhang, Liang Zhang, Shuang Wang, Xuan Cao, Li Ma, Gang Wei, Yingjie Wu, Zhaoyuan Hou
The zinc finger protein Snail is a master regulator of epithelial-mesenchymal transition (EMT) and a strong inducer of tumor metastasis, yet the signal cascades triggered by Snail have not been completely revealed. Here, we report the discovery of the sulfation program that can be induced by Snail in breast cancer cells, and which plays an essential role in cell migration and metastasis. Specifically, Snail induces the expression of PAPSS2, a gene that encodes a rate-limiting enzyme in sulfation pathway, and VCAN, a gene that encodes the chondroitin sulfate proteoglycan Versican in multiple breast cancer cells...
June 28, 2018: Cell Death and Differentiation
Julie-Myrtille Bourgognon, Jereme G Spiers, Hannah Scheiblich, Alexey Antonov, Sophie J Bradley, Andrew B Tobin, Joern R Steinert
Neurodegenerative conditions are characterised by a progressive loss of neurons, which is believed to be initiated by misfolded protein aggregations. During this time period, many physiological and metabolomic alterations and changes in gene expression contribute to the decline in neuronal function. However, these pathological effects have not been fully characterised. In this study, we utilised a metabolomic approach to investigate the metabolic changes occurring in the hippocampus and cortex of mice infected with misfolded prion protein...
June 18, 2018: Cell Death and Differentiation
Y Ge, Y-M Cai, L Bonneau, V Rotari, A Danon, E A McKenzie, H McLellan, L Mach, P Gallois
We thank D Nicholson for initial advice on caspase activity purification and B Turk for advice on recombinant cathepsin B. We thank N Atanasova for cell death assays. The Bioimaging Facility microscopes used in this study were purchased with grants from BBSRC, Wellcome Trust and the University of Manchester Strategic Fund. Special thanks go to D Knight in the Faculty Biomolecular Analysis facility. We thank P Birch and M Kim for improving the manuscript. The project was partially funded by BBSRC Grants 34/P14516, BB/K009478/1 and China National High-Tech Research and Development Programme(863 programme)NO...
June 18, 2018: Cell Death and Differentiation
Mara Livezey, Rui Huang, Paul J Hergenrother, David J Shapiro
The endoplasmic reticulum stress sensor, the unfolded protein response (UPR), regulates intracellular protein homeostasis. While transient activation of the reactive UPR by unfolded protein is protective, prolonged and sustained activation of the reactive UPR triggers CHOP-mediated apoptosis. In the recently characterized, evolutionarily conserved anticipatory UPR, mitogenic hormones and other effectors pre-activate the UPR; how strong and sustained activation of the anticipatory UPR induces cell death was unknown...
June 13, 2018: Cell Death and Differentiation
Mart Bittremieux, Rita M La Rovere, Haidar Akl, Claudio Martines, Kirsten Welkenhuyzen, Kathia Dubron, Myriam Baes, Ann Janssens, Peter Vandenberghe, Luca Laurenti, Katja Rietdorf, Giampaolo Morciano, Paolo Pinton, Katsuhiko Mikoshiba, Martin D Bootman, Dimitar G Efremov, Humbert De Smedt, Jan B Parys, Geert Bultynck
Anti-apoptotic Bcl-2 proteins are upregulated in different cancers, including diffuse large B-cell lymphoma (DLBCL) and chronic lymphocytic leukemia (CLL), enabling survival by inhibiting pro-apoptotic Bcl-2-family members and inositol 1,4,5-trisphosphate (IP3 ) receptor (IP3 R)-mediated Ca2+ -signaling. A peptide tool (Bcl-2/IP3 R Disruptor-2; BIRD-2) was developed to abrogate the interaction of Bcl-2 with IP3 Rs by targeting Bcl-2's BH4 domain. BIRD-2 triggers cell death in primary CLL cells and in DLBCL cell lines...
June 13, 2018: Cell Death and Differentiation
Y Zhang, J Kim, A C Mueller, B Dey, Y Yang, D-H Lee, J Hachmann, S Finderle, D M Park, J Christensen, D Schiff, B Purow, A Dutta, R Abounader
Following publication of the article, the author named as "B Dey", wished to point out that his full name is "Bijan K. Dey". This was not reflected in the typesetting of the article, and as a consequence the article is not visible on Pub Med when a search is conducted on his full name.
June 13, 2018: Cell Death and Differentiation
Shengkai Huang, Yan Li, Xinghua Yuan, Mei Zhao, Jia Wang, You Li, Yuan Li, Hong Lin, Qiao Zhang, Wenjie Wang, Dongdong Li, Xin Dong, Lanfen Li, Min Liu, Weiyan Huang, Changzhi Huang
Ubiquilin4 (Ubqln4), a member of the UbL-UBA protein family, serves as an adaptor in the degradation of specific substrates via the proteasomal pathway. However, the biological function of Ubqln4 remains largely unknown, especially in cancer. Here, we reported that Ubqln4 was downregulated in gastric cancer tissues and functioned as a tumor suppressor by inhibiting gastric cancer cell proliferation in vivo and in vitro. Overexpression of Ubqln4-induced cellular senescence and G1-S cell cycle arrest in gastric cancer cells and activated the p53/p21 axis...
June 13, 2018: Cell Death and Differentiation
Sarah Nicklas, Anna-Lena Hillje, Satoshi Okawa, Ina-Maria Rudolph, Franziska Melanie Collmann, Thea van Wuellen, Antonio Del Sol, Jens C Schwamborn
The balance between stem cell maintenance and differentiation has been proposed to depend on antagonizing ubiquitination and deubiquitination reactions of key stem cell transcription factors (SCTFs) mediated by pairs of E3 ubiquitin ligases and deubiquitinating enzymes. Accordingly, increased ubiquitination results in proteasomal degradation of the SCTF, thereby inducing cellular differentiation, whereas increased deubiquitination stabilizes the SCTF, leading to maintenance of the stem cell fate. In neural stem cells, one of the key SCTFs is c-Myc...
June 13, 2018: Cell Death and Differentiation
Yong Yang, Jie Ren, Yuhao Sun, Yuan Xue, Zhijian Zhang, Aihua Gong, Baofeng Wang, Zhihong Zhong, Zhenwen Cui, Zhiyu Xi, Guo-Yuan Yang, Qingfang Sun, Liuguan Bian
Reactive astrogliosis is a common response to insults to the central nervous system, but the mechanism remains unknown. In this study, we found the temporal and spatial differential expression of glial fibrillary acidic protein (GFAP) and Vimentin in the intracerebral hemorrhage (ICH) mouse brain, indicating that the de-differentiation and astroglial-mesenchymal transition (AMT) of astrocytes might be an early event in reactive astrogliosis. Further we verified the AMT finding in purified astrocyte cultures exposed to hemoglobin (Hb)...
June 7, 2018: Cell Death and Differentiation
Yonglong Chen, Yimin Li, Yougong Peng, Xuan Zheng, Shijie Fan, Yong Yi, Peng Zeng, Hu Chen, Han Kang, Yujun Zhang, Zhi-Xiong Xiao, Chenghua Li
p63 and c-Myc are key transcription factors controlling genes involved in the cell cycle and cellular senescence. We previously reported that p63α can destabilize MM1 protein to derepress c-Myc, resulting in cell cycle progress and tumorigenesis. However, how the proteasomal degradation of MM1 is facilitated remains unclear. In the present study, we identified a novel E3 ligase, HERC3, which can mediate ubiquitination of MM1 and promote its proteasome-dependent degradation. We found that ΔNp63α transcriptionally up-regulates HERC3 and knockdown of HERC3 abrogates ΔNp63α-induced down-regulation of MM1...
June 7, 2018: Cell Death and Differentiation
Chenming Wu, Kuntian Luo, Fei Zhao, Ping Yin, Ying Song, Min Deng, Jinzhou Huang, Yuping Chen, Lei Li, SeungBaek Lee, JungJin Kim, Qin Zhou, Xinyi Tu, Somaira Nowsheen, Qifeng Luo, Xiumei Gao, Zhenkun Lou, Zhongmin Liu, Jian Yuan
β-catenin is a major transcriptional activator of the canonical Wnt/β-catenin signaling pathway. It is important for a series of biological processes including tissue homeostasis, and embryonic development and is involved in various human diseases. Elevated oncogenic activity of β-catenin is frequently observed in cancers, which contributes to survival, metastasis and chemo-resistance of cancer cells. However, the mechanism of β-catenin overexpression in cancers is not well defined. Here we demonstrate that the deubiquitination enzyme USP20 is a new regulator of the Wnt/β-catenin signaling pathway...
June 4, 2018: Cell Death and Differentiation
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