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Wei Wang, Feiyu Liu, Chaoyang Wang, Chengde Wang, Yijun Tang, Zhongmin Jiang
BACKGROUND Src and Fn14 are implicated in the aggressiveness of non-small cell lung cancer (NSCLC) cells, yet the molecular mechanism is not fully understood. MATERIAL AND METHODS The proliferation, migration, and invasion of HCC827 cells with Src knockdown were examined in vitro. The expression of Fn14 and the activation of NF-κB signaling pathway in Src-silenced HCC827 cells were detected by western blot. The role of Fn14 in Src-regulated cell migration/invasion and activation of NF-κB signaling was investigated by overexpressing Fn14 in Src knockdown NSCLC cells...
March 3, 2018: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
David S Hersh, Sen Peng, Jimena G Dancy, Rebeca Galisteo, Jennifer M Eschbacher, Rudy J Castellani, Jonathan E Heath, Teklu Legesse, Anthony J Kim, Graeme F Woodworth, Nhan L Tran, Jeffrey A Winkles
The TNF receptor superfamily member Fn14 is overexpressed by many solid tumor types, including glioblastoma (GBM), the most common and lethal form of adult brain cancer. GBM is notable for a highly infiltrative growth pattern and several groups have reported that high Fn14 expression levels can increase tumor cell invasiveness. We reported previously that the mesenchymal and proneural GBM transcriptomic subtypes expressed the highest and lowest levels of Fn14 mRNA, respectively. Given the recent histopathological re-classification of human gliomas by the World Health Organization based on isocitrate dehydrogenase 1 (IDH1) gene mutation status, we extended this work by comparing Fn14 gene expression in IDH1 wild-type (WT) and mutant (R132H) gliomas and in cell lines engineered to overexpress the IDH1 R132H enzyme...
February 16, 2018: Journal of Neuro-oncology
Vikas Dutt, Vikram Saini, Prachi Gupta, Nirmaljeet Kaur, Manju Bala, Ravindra Gujar, Anita Grewal, Sanjeev Gupta, Anita Dua, Ashwani Mittal
BACKGROUND: Elevated levels of inflammatory molecules are the key players in muscle wasting/atrophy leading to human morbidity. TNFα is a well-known pro-inflammatory cytokine implicated in the pathogenesis of muscle wasting under diverse clinical settings. S-allyl cysteine (SAC), an active component of garlic (Allium sativum), has established anti-oxidant and anti-inflammatory effects in various cell types. However, the impact of SAC on skeletal muscle pathology remains unexplored. Owing to the known anti-inflammatory properties of SAC, we investigate whether pre-treatment with SAC has a protective role in TNFα induced atrophy in cultured myotubes...
December 27, 2017: Biochimica et Biophysica Acta
Feng Guan, Liang Wang, Shuyu Hao, Zhen Wu, Jian Bai, Zhuang Kang, Quan Zhou, Hong Chang, Hui Yin, Da Li, Kaibin Tian, Junpeng Ma, Guijun Zhang, Junting Zhang
Retinol dehydrogenase-10 (RDH10) is a member of the short-chain dehydrogenase/reductase family, which plays an important role in retinoic acid (RA) synthesis. Here, we show that RDH10 is highly expressed in human gliomas, and its expression correlates with tumor grade and patient survival times. In vitro, lentivirus-mediated shRNA knockdown of RDH10 suppressed glioma cell proliferation, survival, and invasiveness and cell cycle progression. In vivo, RDH10 knockdown reduced glioma growth in nude mice. Microarray analysis revealed that RDH10 silencing reduces expression of TNFRSF12A (Fn14), TNFSF12 (TWEAK), TRAF3, IKBKB (IKK-β), and BMPR2, while it increases expression of TRAF1, NFKBIA (IκBα), NFKBIE (IκBε), and TNFAIP3...
December 1, 2017: Oncotarget
Wei-An Chang, Meng-Chi Yen, Jen-Yu Hung, Chih-Jen Yang, Shu-Fang Jian, I-Jeng Yeh, Kuan-Ting Liu, Ya-Ling Hsu, Po-Lin Kuo
Several of the soluble inflammatory molecules such as cytokines and chemokines are involved in the regulation of cancer behaviors. Tumor necrosis factor (TNF)‑like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily and is a ligand of fibroblast growth factor inducible 14 (Fn14). TWEAK/Fn14 signaling pathways promote tumor progression in several types of human cancer. In the present study, we investigated the role of TWEAK through bioinformatic assay, in vitro experiments, and serum levels in patients with non‑small cell lung cancer (NSCLC)...
February 2018: Oncology Reports
Antonio Martínez-Aranda, Vanessa Hernández, Ferran Moreno, Núria Baixeras, Daniel Cuadras, Ander Urruticoechea, Miguel Gil-Gil, Noemí Vidal, Xavier Andreu, Miquel A Seguí, Rosa Ballester, Eva Castella, Angels Sierra
FN14 has been implicated in many intracellular signaling pathways, and GRP94 is a well-known endoplasmic reticulum protein regulated by glucose. Recently, both have been associated with metastasis progression in breast cancer patients. We studied the usefulness of FN14 and GRP94 expression to stratify breast cancer patients according their risk of brain metastasis (BrM) progression. We analyzed FN14 and GRP94 by immunohistochemistry in a retrospective multicenter study using tissue microarrays from 208 patients with breast carcinomas, of whom 52 had developed BrM...
2017: Frontiers in Oncology
Audrey Boulamery, Sophie Desplat-Jégo
Observed in many central nervous system diseases, neuroinflammation (NI) proceeds from peripheral immune cell infiltration into the parenchyma, from cytokine secretion and from oxidative stress. Astrocytes and microglia also get activated and proliferate. NI manifestations and consequences depend on its context and on the acute or chronic aspect of the disease. The tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/Fn14 pathway has been involved in chronic human inflammatory pathologies such as neurodegenerative, autoimmune, or malignant diseases...
2017: Frontiers in Immunology
Xiaoying Chen, Vahid Farrokhi, Pratap Singh, Mireia Fernandez Ocana, Jenil Patel, Lih-Ling Lin, Hendrik Neubert, Joanne Brodfuehrer
Discovery of the upregulation of fibroblast growth factor-inducible-14 (Fn14) receptor following tissue injury has prompted investigation into biotherapeutic targeting of the Fn14 receptor for the treatment of conditions such as chronic kidney diseases. In the development of monoclonal antibody (mAb) therapeutics, there is an increasing trend to use biomeasures combined with mechanistic pharmacokinetic/pharmacodynamic (PK/PD) modeling to enable decision making in early discovery. With the aim of guiding preclinical efforts on designing an antibody with optimized properties, we developed a mechanistic site-of-action (SoA) PK/PD model for human application...
January 2018: MAbs
Cuimin Zhu, Leguo Zhang, Zhiming Liu, Chen Li, Yajie Bai
Asthma, an increasingly common chronic disease among children, are characterized by airway remodeling, which is partly attributed to the proliferation and migration of airway smooth muscle cell (ASMC). The purpose of the present study was to investigate potential roles and mechanisms of the tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/fibroblast growth factor-inducible molecule 14 (Fn14) axis on cell proliferation and migration in HASMCs. Compared to HASMCs from non-asthmatic patients, those from asthmatic patients showed elevated expression levels of both Fn14 and TWEAK...
November 16, 2017: Journal of Cellular Biochemistry
Ting Xu, Yan Yang, Li Zhao, Dan-Dan Zhou, Yan Zhang
OBJECTIVE: To investigate the expression of tumor necrosis factor-like weak inducer of apoptosis (TWEAK)/ fibroblast growth factorinducible 14 (Fn14) in the serum and colon tissue of Crohn's disease (CD) and to elucidate whether the expression of TWEAK/Fn14 can be used as an indicator for intestinal fibrosis. METHODS: Blood samples from 67 CD patients and 33 healthy controls were collected to measure the level of TWEAK by ELISA. Meanwhile,colon samples from 29 CD patients received colectomy and the normal colon tissues from 15 patients with colon cancer were included...
September 2017: Sichuan da Xue Xue Bao. Yi Xue Ban, Journal of Sichuan University. Medical Science Edition
Qilu Liu, Shengxiang Xiao, Yumin Xia
Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor-fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-κB signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10...
2017: Mediators of Inflammation
Xuening Wang, Shengxiang Xiao, Yumin Xia
Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor-inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators...
2017: Cellular Physiology and Biochemistry
Yong Guo, Yuanjiang Liao
Immunoglobulin A nephropathy (IgAN) is one of the most common glomerular diseases worldwide. Various studies have identified a host of microRNAs (miRNAs) abnormally expressed in IgAN and might affect the pathogenesis and progression of IgAN. However, miR-200bc/429 cluster in the pathopoiesis of IgAN remains poorly understood. For this study, we found that miR-200bc/429 cluster is downregulated in IgAN tissues and IgAN podocytes and HK2 cells compared with their matched controls respectively. In addition, overexpression of miR-200bc/429 cluster in IgAN podocytes and HK2 cells could attenuate the release of inflammatory cytokines MCP-1, IL-6 and RANTES...
November 2017: International Immunopharmacology
Yingying Dong, Yi Zhang, Linlin Xia, Ping Wang, Jingyun Chen, Meifeng Xu, Xingyin Liu, Yumin Xia
Anti-DNA IgG is a hallmark of systemic lupus erythematosus and induces internal injuries in patients. It is known that cutaneous lupus erythematosus (CLE) involves the deposition of autoantibodies in the dermoepidermal junction of the skin and that anti-DNA IgG binds specifically to keratinocytes. However, the definite role of anti-DNA IgG in CLE remains unclear. The purpose of this study was to elucidate the effect of anti-DNA IgG on keratinocytes in CLE. Skin tissues were collected from patients with CLE and healthy controls...
September 9, 2017: Immunology Letters
Aniket S Wadajkar, Jimena G Dancy, Nathan B Roberts, Nina P Connolly, Dudley K Strickland, Jeffrey A Winkles, Graeme F Woodworth, Anthony J Kim
The most common and deadly form of primary brain cancer, glioblastoma (GBM), is characterized by significant intratumoral heterogeneity, microvascular proliferation, immune system suppression, and brain tissue invasion. Delivering effective and sustained treatments to the invasive GBM cells intermixed with functioning neural elements is a major goal of advanced therapeutic systems for brain cancer. Previously, we investigated the nanoparticle characteristics that enable targeting of invasive GBM cells. This revealed the importance of minimizing non-specific binding within the relatively adhesive, 'sticky' microenvironment of the brain and brain tumors in particular...
December 10, 2017: Journal of Controlled Release: Official Journal of the Controlled Release Society
Manoel Benício Teixeira Ribeiro, Vinicius Guzzoni, Jeffrey M Hord, Gisele Nunes Lopes, Rita de Cássia Marqueti, Rosângela Vieira de Andrade, Heloisa Sobreiro Selistre-de-Araujo, João Luiz Q Durigan
Sarcopenia is a complex multifactorial process, some of which involves fat infiltration. Intramyocellular lipid (IMCL) accumulation is postulated to play a role on sarcopenia during aging, which is believed to be due alterations in glucose homeostasis in the skeletal muscle. Sarcopenia, along with intramuscular lipids, is associated with physical inactivity. Resistance training (RT) has been indicated to minimize the age-induced muscle skeletal adaptations. Thus, we aimed to investigate the effects of RT on mRNA levels of regulatory components related to intramyocellular lipid, glucose metabolism and fiber size in soleus and gastrocnemius muscles of aged rats...
August 17, 2017: Scientific Reports
Zhuoxuan Li, Jing Xie, Shan Peng, Sha Liu, Ying Wang, Weiyue Lu, Jie Shen, Chong Li
The development of proteolysis-resistant d-peptide ligands for targeted drug/gene delivery has been greatly limited, due to the challenge that lies in the chemical synthesis of membrane receptors without altering their structures. In the present research, a novel strategy utilizing self-stabilized extracellular CRD of the membrane receptor was developed to construct d-peptide ligands and their mediated targeted drug delivery systems. Fn14, a cell surface receptor overexpressed in many cancers including pancreatic and triple-negative breast cancers, was selected as the model receptor...
August 16, 2017: Bioconjugate Chemistry
Guanglei Hu, Weihui Zeng, Yumin Xia
TWEAK (tumor necrosis factor-related weak inducer of apoptosis), a member of the tumor necrosis factor superfamily, acts on cells by binding to its only receptor named Fn14 (fibroblast growth factor-inducible 14). Their engagement activates a number of intracellular signal transduction cascades and consequently leads to cell death, proliferation, migration, or survival depending on the cellular contexts. Studies have indicated that the expression of TWEAK and Fn14 is upregulated in many solid tumors compared with healthy tissues...
June 2017: Tumour Biology: the Journal of the International Society for Oncodevelopmental Biology and Medicine
Shiqiao Peng, Xiaohui Yu, Xuemin Zhao, Xinyi Wang, Xuren Sun, Cheng Han, Zhongyan Shan, Chenyan Li, Weiping Teng
BACKGROUND: TNF-like weak inducer of apoptosis (TWEAK), its receptor fibroblast growth factor-inducible 14 (Fn14) and its scavenger receptor CD163 (sCD163) have known associations with many autoimmune diseases. However, the role of the TWEAK axis in autoimmune thyroid disease (AITD) remains unclear. Therefore, the aim of this study was to investigate the role of the TWEAK-Fn14 axis in the pathogenesis of AITD. METHODS: Serum levels of soluble TWEAK (sTWEAK) and sCD163 were measured in 38 patients with Graves' disease (GD), 40 patients with Hashimoto's thyroiditis (HT) and 40 healthy controls (HCs)...
June 21, 2017: Clinical Endocrinology
Yale Liu, Meifeng Xu, Xiaoyun Min, Kunyi Wu, Ting Zhang, Ke Li, Shengxiang Xiao, Yumin Xia
Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) binds to its sole receptor fibroblast growth factor-inducible 14 (Fn14), participating in various inflammatory responses. Recently, TWEAK/Fn14 activation was found prominent in the lesions of cutaneous lupus erythematosus (CLE). This study was designed to further reveal the potential role of this pathway in Ro52-mediated photosensitization. TWEAK, Fn14, and Ro52 were determined in the skin lesions of patients with CLE. Murine keratinocytes received ultraviolet B (UVB) irradiation or plus TWEAK stimulation and underwent detection for Ro52 and proinflammatory cytokines...
2017: Frontiers in Immunology
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