Emodin induced necroptosis in the glioma cell line U251 via the TNF- α/RIP1/RIP3 pathway

This study aimed to investigate the effects and mechanisms of emodin-induced necroptosis in the glioma cell line U251 by targeting the TNF- α/RIP1/RIP3 signaling pathway. We found that emodin could significantly inhibit U251 cell proliferation, and the viability of U251 cells treated with emodin was reduced in a dose- and time-dependent manner. Flow cytometry assays and Hoechst-PI staining assays showed that emodin induced apoptosis an d necroptosis. Real-time PCR and western blot analysis showed that emodin upregulated the levels of TNF-α, RIP1, RIP3 and MLKL. Furthermore, the RIP1 inhibitor Nec-1 and the RIP3 inhibitor GSK872 attenuated the killing effect of emodin on U251 cells. In addition, emodin could increase the levels of TNF-α, RIP1, RIP3 and MLKL in vivo. The results demonstrate that emodin could induce necroptosis in glioma possibly through the activation of the TNF-α/RIP1/RIP3 axis. These studies provide novel insight into the induction of necroptosis by emodin and indicate that emodin might be a potential can didate for treating glioma through the necroptosis pathway.
Source: Investigational New Drugs - Category: Drugs & Pharmacology Source Type: research

Related Links:

Alla S. Koltsova1,2, Anna A. Pendina1, Olga A. Efimova1*, Olga G. Chiryaeva1, Tatyana V. Kuznetzova1 and Vladislav S. Baranov1,2 1D.O. Ott Research Institute of Obstetrics, Gynecology and Reproductology, Saint Petersburg, Russia 2Department of Genetics and Biotechnology, Saint Petersburg State University, Saint Petersburg, Russia In the present review, we focus on the phenomenon of chromothripsis, a new type of complex chromosomal rearrangements. We discuss the challenges of chromothripsis detection and its distinction from other chromoanagenesis events. Along with already known causes and mechanisms, we introdu...
Source: Frontiers in Genetics - Category: Genetics & Stem Cells Source Type: research
Conclusions Several model systems are now available to characterize the MSC-tumour interplay in the TME. These offer early promise in establishing robust preclinical platforms for the identification of crucial molecular pathways and for the assessment of clinical efficacy of novel drugs to inhibit cancer development and progression. However, selection of the right model for a given study should be shaped on the purpose, and should also consider fixed biological, biochemical, and biophysical parameters according to the specific tumour type. Finally, in order to get reliable and useful results to be translated to the clinic...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
In conclusion, our WGCNA analysis identified candidate prognostic biomarkers for further basic and clinical researches. Introduction Breast cancer is a frequently diagnosed malignancy and the leading cause of cancer death among females around the world, accounting for 24% of cancer diagnoses and 15% of cancer deaths in females. According to Global Cancer Statistics 2018, there will be nearly 2.1 million new cases diagnosed globally, with ~62 thousand deaths. The incident rates of breast cancer increased in most developing countries during last decades, resulting from a combination of social and economic factors, incl...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
Conclusion: Taken together, lncRNA OIP5-AS1 acted as a ceRNA to drive proliferation, migration and invasion of HemECs through regulating miR-195-5p/NOB1 axis. Introduction Infant hemangioma (IH) is a benign neoplasm commonly seen in childhood, which is more common in premature infants and infants with low birth weight (Smith et al., 2017). There are three distinct clinical histological stages in IH: the early proliferative stage, when undeveloped blood vessels are rapidly growing; plateau stage and final regressive stage, with scattered capillaries and large drainage vessels (Csoma et al., 2017). IH is characterize...
Source: Frontiers in Pharmacology - Category: Drugs & Pharmacology Source Type: research
Gui-Jiang Wei1,2, Ming-Qing Yuan1, Li-He Jiang1, Yu-Lan Lu3, Chun-Hong Liu3, Hong-Cheng Luo3, Hua-Tuo Huang3, Zong-Quan Qi1* and Ye-Sheng Wei1,2* 1Department of Cell Biology, Medical College of Guangxi University, Nanning, China 2Department of Medical Laboratory, Affiliated Hospital of Guilin Medical University, Guilin, China 3Department of Medical Laboratory, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, China miRNAs are small non-coding RNAs modulating gene expression, and variants in miRNA genes are involved in the pathogenesis of ischemic stroke (IS). However, the effect of mi...
Source: Frontiers in Physiology - Category: Physiology Source Type: research
Qiancheng Deng1, Yangyang Luo1,2, Christopher Chang3, Haijing Wu1, Yan Ding4* and Rong Xiao1* 1Hunan Key Laboratory of Medical Epigenetics, Department of Dermatology, The Second Xiangya Hospital, Central South University, Changsha, China 2Department of Dermatology, Hunan Children's Hospital, Changsha, China 3Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, Davis, CA, United States 4Department of Dermatology, Hainan Provincial Dermatology Disease Hospital, Haikou, China Autoimmune diseases are usually complex and multifactorial, characterized by aberrant produc...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
In conclusion, our results of bioinformatic analysis, in vitro and in vivo functional analysis suggested that REST may serve as a promoter of metastasis in pancreatic cancer. Introduction Pancreatic cancer, ranked fourth in cancer-related mortality, is characterized by its rapid progression and early metastasis (1). Patients are hardly cured by surgical resection due to the existing local invasion and distant metastasis (2). Elevating the overall survival rate for pancreatic cancer requires further elucidation of the underlying molecular mechanism of its metastasis. Epithelial-mesenchymal transition (EMT), especially...
Source: Frontiers in Oncology - Category: Cancer & Oncology Source Type: research
In conclusion, osmotic burst of inflated complement-damaged cells may occur, but these bursts are most likely a consequence of metabolic collapse of the cell rather than the cause of cell death. The Complement Cell Death Mediator: A Concerted Action of Toxic Moieties Membrane pores caused by complement were first visualized by electron microscopy on red blood cell membranes as large ring structures (22). Similar lesions were viewed on E. coli cell walls (23). Over the years, ample information on the fine ultrastructure of the MAC that can activate cell death has been gathered (24) and has been recently further examined (...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
Abstract Human NIN1/RPN12 binding protein 1 homolog (NOB1), an RNA binding protein, is expressed ubiquitously in normal tissues such as the lung, liver, and spleen. Its core physiological function is to regulate protease activities and participate in maintaining RNA metabolism and stability. NOB1 is overexpressed in a variety of cancers, including pancreatic cancer, non-small cell lung cancer, ovarian cancer, prostate carcinoma, osteosarcoma, papillary thyroid carcinoma, colorectal cancer, and glioma. Although existing data indicate that NOB1 overexpression is associated with cancer growth, invasion, and poor prog...
Source: Current Drug Targets - Category: Drugs & Pharmacology Authors: Tags: Curr Drug Targets Source Type: research
In conclusion, HOXD-AS1 may be considered as a promising diagnostic/prognostic biomarker or a novel therapeutic target for cancers.
Source: Clinica Chimica Acta - Category: Laboratory Medicine Source Type: research
More News: Bone Cancers | Brain Tumor | Cancer | Cancer & Oncology | China Health | Drugs & Pharmacology | Glioma | Investigational New Drugs | Liver | Osteosarcoma | Prostate Cancer | Rhubarb | Study | Urology & Nephrology