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Cell Death & Disease

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https://www.readbyqxmd.com/read/30341286/targeting-enhancer-of-zeste-homolog-2-protects-against-acute-kidney-injury
#1
X Zhou, X Zang, Y Guan, T Tolbert, T C Zhao, G Bayliss, S Zhuang
Despite the established oncogenic and profibrotic functions of enhancer of zeste homolog 2 (EZH2), a methyltransferase that induces histone H3 lysine 27 trimethylation (H3K27me3), its role in acute kidney injury (AKI) remains unclear. In this study, we demonstrated that EZH2 and H3K27me3 were upregulated in the murine kidney with AKI induced by either ischemia-reperfusion (I/R) or folic acid (FA). Pharmacologic inhibition of EZH2 with 3-deazaneplanocin A (3-DZNeP) prevented tubular injury in both models as demonstrated by reduced renal dysfunction, diminished neutrophil gelatinase-associated lipocalin expression and decreased renal tubular cell death...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341285/diesel-exhaust-particles-induce-autophagy-and-citrullination-in-normal-human-bronchial-epithelial-cells
#2
Tania Colasanti, Silvana Fiorito, Cristiano Alessandri, Annalucia Serafino, Federica Andreola, Cristiana Barbati, Francesca Morello, Michela Alfè, Gabriele Di Blasio, Valentina Gargiulo, Marta Vomero, Fabrizio Conti, Guido Valesini
A variety of environmental agents has been found to influence the development of autoimmune diseases; in particular, the studies investigating the potential association of systemic autoimmune rheumatic diseases with environmental micro and nano-particulate matter are very few and contradictory. In this study, the role of diesel exhaust particles (DEPs), one of the most important components of environment particulate matter, emitted from Euro 4 and Euro 5 engines in altering the Normal Human Bronchial Epithelial (NHBE) cell biological activity was evaluated...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341284/activation-of-the-interferon-type-i-response-rather-than-autophagy-contributes-to-myogenesis-inhibition-in-congenital-dm1-myoblasts
#3
Milena Rizzo, Pascale Beffy, Renata Del Carratore, Alessandra Falleni, Virginia Pretini, Romina D'Aurizio, Annalisa Botta, Monica Evangelista, Andrea Stoccoro, Fabio Coppedè, Denis Furling, Marcella Simili
Congenital myotonic dystrophy type 1 (CDM1) is characterized by severe symptoms that affect patients from birth, with 40% mortality in the neonatal period and impaired skeletal muscle development. In this paper, we examined the relationship between autophagy and abnormal myogenic differentiation of CDM1 myoblasts. We investigated these pathological features at both ultrastructural and molecular levels, utilizing two CDM1 foetal myoblasts, CDM13 and CDM15, with 1800 and 3200 repeats, respectively. The congenital nature of these CDM1 myoblasts was confirmed by the high methylation level at the DMPK locus...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341283/microrna-495-3p-inhibits-multidrug-resistance-by-modulating-autophagy-through-grp78-mtor-axis-in-gastric-cancer
#4
Sheng Chen, Jian Wu, Kai Jiao, Qiong Wu, Jiaojiao Ma, Di Chen, Jianqin Kang, Guodong Zhao, Yongquan Shi, Daiming Fan, Guohong Zhao
Multidrug resistance (MDR) accounts for poor prognosis in gastric cancer (GC). MicroRNAs (miRNAs) are critical regulators of MDR via modulation of the target genes. The present study revealed that miR-495-3p could act via a target gene, GRP78, to regulate the process of autophagy and inhibit MDR. Based on the in vitro and in vivo gain-of-function or loss-of-function experiments, overexpression of miR-495-3p was sufficient to reverse the MDR to four chemotherapeutics in vitro and inhibit the tumor growth in vivo...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341282/ampk-dependent-autophagy-upregulation-serves-as-a-survival-mechanism-in-response-to-tumor-treating-fields-ttfields
#5
Anna Shteingauz, Yaara Porat, Tali Voloshin, Rosa S Schneiderman, Mijal Munster, Einav Zeevi, Noa Kaynan, Karnit Gotlib, Moshe Giladi, Eilon D Kirson, Uri Weinberg, Adrian Kinzel, Yoram Palti
Tumor Treating Fields (TTFields), an approved treatment modality for glioblastoma, are delivered via non-invasive application of low-intensity, intermediate-frequency, alternating electric fields. TTFields application leads to abnormal mitosis, aneuploidy, and increased cell granularity, which are often associated with enhancement of autophagy. In this work, we evaluated whether TTFields effected the regulation of autophagy in glioma cells. We found that autophagy is upregulated in glioma cells treated with TTFields as demonstrated by immunoblot analysis of the lipidated microtubule-associated protein light chain 3 (LC3-II)...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341281/a-functional-genomics-screen-reveals-a-strong-synergistic-effect-between-docetaxel-and-the-mitotic-gene-dlgap5-that-is-mediated-by-the-androgen-receptor
#6
Kay Hewit, Emma Sandilands, Rafael Sanchez Martinez, Daniel James, Hing Y Leung, David M Bryant, Emma Shanks, Elke K Markert
Based on a molecular classification of prostate cancer using gene expression pathway signatures, we derived a set of 48 genes in critical pathways that significantly predicts clinical outcome in all tested patient cohorts. We tested these genes in a functional genomics screen in a panel of three prostate cancer cell lines (LNCaP, PC3, DU145), using RNA interference. The screen revealed several genes whose knockdown caused strong growth inhibition in all cell lines. Additionally, we tested the gene set in the presence of docetaxel to see whether any gene exhibited additive or synergistic effects with the drug...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341280/mir4673-improves-fitness-profile-of-neoplastic-cells-by-induction-of-autophagy
#7
Kağan Dökümcü, Mary Simonian, Ramin M Farahani
Therapeutic resistance of neoplasms is mainly attributed to gradual evolution of mutational profile1 . Here, we demonstrate a microRNA-mediated mechanism that effectively improves fitness of SKBR3 mammary carcinoma cells by cytoplasmic reprogramming. The reprogramming is triggered by endogenous miR4673 transcribed from notch-1 locus. The miRNA downregulates cdk-18, a cyclin-dependent kinase that regulates M-G1 transition in cycling cells2,3 . Suppression of cdk-18 triggers mitophagy and autophagy. Due to high autophagic flux, oestrogen receptor-1+ /progesterone receptor+ /p53+ (Esr1+ /Pr+ /p53+ ) SKBR3 cells are coerced into an Esr1- /Prlow /p53- profile...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30341279/loss-of-grhl3-leads-to-tarc-ccl17-mediated-keratinocyte-proliferation-in-the-epidermis
#8
Stephen J Goldie, Denny L Cottle, Fiona H Tan, Suraya Roslan, Seema Srivastava, Rhys Brady, Darren D Partridge, Alana Auden, Ian M Smyth, Stephen M Jane, Sebastian Dworkin, Charbel Darido
Identifying soluble factors that influence epidermal integrity is critical for the development of preventative and therapeutic strategies for disorders such as ichthyosis, psoriasis, dermatitis and epidermal cancers. The transcription factor Grainyhead-like 3 (GRHL3) is essential for maintaining barrier integrity and preventing development of cutaneous squamous cell carcinoma (SCC); however, how loss of this factor, which in the skin is expressed exclusively within suprabasal epidermal layers triggers proliferation of basal keratinocytes, had thus far remained elusive...
October 19, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30337536/autophagy-suppresses-self-renewal-ability-and-tumorigenicity-of-glioma-initiating-cells-and-promotes-notch1-degradation
#9
Zhennan Tao, Tao Li, Haiwen Ma, Yihan Yang, Chen Zhang, Long Hai, Peidong Liu, Feng Yuan, Jiabo Li, Li Yi, Luqing Tong, Yingshuai Wang, Yang Xie, Haolang Ming, Shengping Yu, Xuejun Yang
Autophagy is a vital process that involves degradation of long-lived proteins and dysfunctional organelles and contributes to cellular metabolism. Glioma-initiating cells (GICs) have the ability to self-renew, differentiate into heterogeneous types of tumor cells, and sustain tumorigenicity; thus, GICs lead to tumor recurrence. Accumulating evidence indicates that autophagy can induce stem cell differentiation and increase the lethality of temozolomide against GICs. However, the mechanism underlying the regulation of GIC self-renewal by autophagy remains uncharacterized...
October 18, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30337526/btk-a-two-faced-effector-in-cancer-and-tumour-suppression
#10
Miran Rada, Nickolai Barlev, Salvador Macip
Many genes of the human genome display pleiotropic activity, playing an important role in two or more unrelated pathways. Surprisingly, some of these functions can even be antagonistic, often letting to divergent functional outcomes depending on microenviromental cues and tissue/cell type-dependent parameters. Lately, the Bruton's tyrosine kinase (BTK) has emerged as one of such pleiotropic genes, with opposing effects in cancer pathways. While it has long been considered oncogenic in the context of B cell malignancies, recent data shows that BTK can also act as a tumour suppressor in other cells, as an essential member of the p53 and p73 responses to damage...
October 18, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30337520/cancer-associated-fibroblasts-promote-progression-and-gemcitabine-resistance-via-the-sdf-1-satb-1-pathway-in-pancreatic-cancer
#11
Lusheng Wei, Huilin Ye, Guolin Li, Yuanting Lu, Quanbo Zhou, Shangyou Zheng, Qing Lin, Yimin Liu, Zhihua Li, Rufu Chen
Cancer-associated fibroblasts (CAFs), a dominant component of the pancreatic tumor microenvironment, are mainly considered as promotors of malignant progression, but the underlying molecular mechanism remains unclear. Here, we show that SDF-1 secreted by CAFs stimulates malignant progression and gemcitabine resistance in pancreatic cancer, partially owing to paracrine induction of SATB-1 in pancreatic cancer cells. CAF-secreted SDF-1 upregulated the expression of SATB-1 in pancreatic cancer cells, which contributed to the maintenance of CAF properties, forming a reciprocal feedback loop...
October 18, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30337519/ylt-11-a-novel-plk4-inhibitor-inhibits-human-breast-cancer-growth-via-inducing-maladjusted-centriole-duplication-and-mitotic-defect
#12
Qian Lei, Lu Xiong, Yong Xia, Zhanzhan Feng, Tiantao Gao, Wei Wei, Xuejiao Song, Tinghong Ye, Ningyu Wang, Cuiting Peng, Zhongping Li, Zhihao Liu, Luoting Yu
Polo-like kinase 4 (PLK4) is indispensable for precise control of centriole duplication. Abnormal expression of PLK4 has been reported in many human cancers, and inhibition of PLK4 activity results in their mitotic arrest and apoptosis. Therefore, PLK4 may be a valid therapeutic target for antitumor therapy. However, clinically available small-molecule inhibitors targeting PLK4 are deficient and their underlying mechanisms still remain not fully clear. Herein, the effects of YLT-11 on breast cancer cells and the associated mechanism were investigated...
October 18, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333561/down-regulation-of-hpgd-by-mir-146b-3p-promotes-cervical-cancer-cell-proliferation-migration-and-anchorage-independent-growth-through-activation-of-stat3-and-akt-pathways
#13
Shuihong Yao, Jingyun Xu, Kaixuan Zhao, Pengxia Song, Qin Yan, Weifei Fan, Wan Li, Chun Lu
While the application of early screening and HPV vaccines has reduced the incidence and mortality rates of cervical cancer, it remains the third most common carcinoma and fourth leading cause of cancer-associated death among women worldwide. The precise mechanisms underlying progression of cervical cancer are not fully understood at present. Here, we detected significant down-regulation of 15-hydroxyprostaglandin dehydrogenase (HPGD) in cervical cancer tissues. Overexpression of HPGD inhibited cervical cancer cell proliferation, migration and anchorage-independent growth to a significant extent...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333529/efferocytosis-of-apoptotic-alveolar-epithelial-cells-is-sufficient-to-initiate-lung-fibrosis
#14
Kevin K Kim, Megan R Dotson, Manisha Agarwal, Jibing Yang, Patrick B Bradley, Natalia Subbotina, John J Osterholzer, Thomas H Sisson
Type II alveolar epithelial cell (AEC) apoptosis is a prominent feature of fibrotic lung diseases and animal models of pulmonary fibrosis. While there is growing recognition of the importance of AEC injury and apoptosis as a causal factor in fibrosis, the underlying mechanisms that link these processes remain unknown. We have previously shown that targeting the type II alveolar epithelium for injury by repetitively administering diphtheria toxin to transgenic mice expressing the diphtheria toxin receptor off of the surfactant protein C promoter (SPC-DTR) develop lung fibrosis, confirming that AEC injury is sufficient to cause fibrosis...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333481/mina53-deficiency-leads-to-glioblastoma-cell-apoptosis-via-inducing-dna-replication-stress-and-diminishing-dna-damage-response
#15
Fan Xuan, Mengying Huang, Erhu Zhao, Hongjuan Cui
MYC-induced nuclear antigen (MINA53) is a JmjC (jumonji C domain)-containing protein, which is highly expressed in many cancers including glioblastoma. We have revealed in our previous report that MINA53 is a poor prognostic indicator for glioblastoma patients, and knockdown of MINA53 could reduce glioblastoma malignancy. In this study, we found that MINA53 knockdown could decrease the DNA replication initiation in glioblastoma cells. Through further investigations, we revealed that MINA53 could regulate the expression of the CDC45-MCM-GINS (CMG) complex genes, which are vital for DNA replication initiation...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333480/tumor-suppressive-mir-6775-3p-inhibits-escc-progression-through-forming-a-positive-feedback-loop-with-p53-via-mage-a-family-proteins
#16
Lingjiao Meng, Fei Liu, Yingchao Ju, Pingan Ding, Sihua Liu, Sheng Chang, Shina Liu, Yi Zhang, Yishui Lian, Lina Gu, Xiaochong Zhang, Meixiang Sang
Accumulating evidences indicate that microRNAs (miRNAs) play vital roles in multiple diseases, including cancer. In the present study, we showed that miR-6775-3p plays a tumor suppressive role in esophageal squamous cell carcinoma (ESCC). High expression miR-6775-3p is associated with good clinical outcomes of ESCC patients. Over-expression of miR-6775-3p inhibited tumor growth and liver metastasis of ESCC xenograft tumors. Enforced expression of miR-6775-3p inhibited ESCC cell proliferation, migration, and invasion...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333479/transgenic-overexpression-of-furin-increases-epileptic-susceptibility
#17
Yi Yang, Miaoqing He, Xin Tian, Yi Guo, Feng Liu, Yun Li, Haiqing Zhang, Xi Lu, Demei Xu, Ruijiao Zhou, Yuanlin Ma, Wei Wang, Guojun Chen, Yida Hu, Xuefeng Wang
The proprotein convertase Furin plays crucial roles in the pathology of many diseases. However, the specific role of furin in epilepsy remains unclear. In our study, furin protein was increased in the temporal neocortex of epileptic patients and in the hippocampus and cortex of epileptic mice. The furin transgenic (TG) mice showed increased susceptibility to epilepsy and heightened epileptic activity compared with wild-type (WT) mice. Conversely, lentivirus-mediated knockdown of furin restrained epileptic activity...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333478/mir-3178-inhibits-cell-proliferation-and-metastasis-by-targeting-notch1-in-triple-negative-breast-cancer
#18
Peng Kong, Lie Chen, Muxin Yu, Jing Tao, Jiawei Liu, Yue Wang, Hong Pan, Wenbin Zhou, Shui Wang
Triple-negative breast cancer (TNBC) has a poorer outcome than other subtypes of breast cancer, and the discovery of dysregulated microRNA (miRNA) and their role in tumor progression has provided a new avenue for elucidating the mechanism involved in TNBC. In this study, we identified that miR-3178 was significantly reduced in TNBC, and the low miR-3178 expression correlated with poor overall survival in TNBC but not in non-TNBC. The ectopic overexpression of miR-3178 suppressed TNBC cell proliferation, invasion, and migration by inhibiting the epithelial-to-mesenchymal (EMT) transition...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333477/inhibiting-repulsive-guidance-molecule-a-suppresses-secondary-progression-in-mouse-models-of-multiple-sclerosis
#19
Shogo Tanabe, Yuki Fujita, Kaori Ikuma, Toshihide Yamashita
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system that is characterized by motor deficits, fatigue, pain, cognitive impairment, and sensory and visual dysfunction. Secondary progressive multiple sclerosis (SPMS) is a progressive form of MS that develops from relapsing-remitting MS. Repulsive guidance molecule-a (RGMa) has diverse functions, including axon growth inhibition and immune regulation. Here, we show inhibiting RGMa had therapeutic effects in mouse models of SPMS. We induced experimental autoimmune encephalomyelitis in nonobese diabetic mice (NOD-EAE mice) and treated them with humanized anti-RGMa monoclonal antibody...
October 17, 2018: Cell Death & Disease
https://www.readbyqxmd.com/read/30333475/carbon-monoxide-induced-tfeb-nuclear-translocation-enhances-mitophagy-mitochondrial-biogenesis-in-hepatocytes-and-ameliorates-inflammatory-liver-injury
#20
Hyo Jeong Kim, Yeonsoo Joe, So-Young Rah, Seul-Ki Kim, Se-Ung Park, Jeongmin Park, Jin Kim, Jinhyun Ryu, Gyeong Jae Cho, Young-Joon Surh, Stefan W Ryter, Uh-Hyun Kim, Hun Taeg Chung
Carbon monoxide (CO) can confer protection against cellular stress, whereas the potential involvement of autophagy and lysosomal biogenesis remains incompletely understood. We demonstrate here that the activation of protein kinase R (PKR)-like endoplasmic reticulum (ER) kinase (PERK) with CO increased the nuclear translocation of transcription factor EB (TFEB). PERK activation by CO increased intracellular Ca2+ concentration and the phosphatase activity of calcineurin against TFEB. Moreover, we found that in the deficiency of TFEB, CO not only failed to recruit Parkin to the mitochondria but also failed to increase expression of lysosomal genes such as Lamp1, CathB, and TPP1...
October 17, 2018: Cell Death & Disease
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