Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells: an in vitro and in vivo study
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Title
Celastrol induces apoptosis and autophagy via the ROS/JNK signaling pathway in human osteosarcoma cells: an in vitro and in vivo study
Authors
Keywords
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Journal
Cell Death & Disease
Volume 6, Issue 1, Pages e1604-e1604
Publisher
Springer Nature
Online
2015-01-22
DOI
10.1038/cddis.2014.543
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Note: Only part of the references are listed.- Inhibition of Autophagy Strengthens Celastrol-Induced Apoptosis in Human Pancreatic Cancer In Vitro and In Vivo Models
- (2014) X. Zhao et al. CURRENT MOLECULAR MEDICINE
- The Chinese Herb Isolate Yuanhuacine (YHL-14) Induces G2/M Arrest in Human Cancer Cells by Up-regulating p21 Protein Expression through an p53 Protein-independent Cascade
- (2014) Ruowen Zhang et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- Activation of p38/JNK Pathway Is Responsible for Embelin Induced Apoptosis in Lung Cancer Cells: Transitional Role of Reactive Oxygen Species
- (2014) Deepa R. Avisetti et al. PLoS One
- Celastrol protects human neuroblastoma SH-SY5Y cells from rotenone-induced injury through induction of autophagy
- (2013) Yong-Ning Deng et al. NEUROCHEMISTRY INTERNATIONAL
- Current Therapeutic Strategies and Novel Approaches in Osteosarcoma
- (2013) Kosei Ando et al. Cancers
- Celastrol inhibits growth and induces apoptotic cell death in melanoma cells via the activation ROS-dependent mitochondrial pathway and the suppression of PI3K/AKT signaling
- (2012) Ju-Hye Lee et al. APOPTOSIS
- Celastrol Suppresses Growth and Induces Apoptosis of Human Hepatocellular Carcinoma through the Modulation of STAT3/JAK2 Signaling Cascade In Vitro and In Vivo
- (2012) P. Rajendran et al. Cancer Prevention Research
- Paraptosis accompanied by autophagy and apoptosis was induced by celastrol, a natural compound with influence on proteasome, ER stress and Hsp90
- (2012) Wen-Bo Wang et al. JOURNAL OF CELLULAR PHYSIOLOGY
- Celastrol inhibits tumor cell proliferation and promotes apoptosis through the activation of c-Jun N-terminal kinase and suppression of PI3 K/Akt signaling pathways
- (2011) Radhamani Kannaiyan et al. APOPTOSIS
- Caspase-8 and Bid: Caught in the act between death receptors and mitochondria
- (2011) Chahrazade Kantari et al. BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
- Celastrol Attenuates Hypertension-Induced Inflammation and Oxidative Stress in Vascular Smooth Muscle Cells via Induction of Heme Oxygenase-1
- (2010) X. Yu et al. AMERICAN JOURNAL OF HYPERTENSION
- Celastrol isolated from Tripterygium regelii induces apoptosis through both caspase-dependent and -independent pathways in human breast cancer cells
- (2010) Hee-Sun Yang et al. FOOD AND CHEMICAL TOXICOLOGY
- HSP90 inhibitor, celastrol, arrests human monocytic leukemia cell U937 at G0/G1 in thiol-containing agents reversible way
- (2010) Bin Peng et al. Molecular Cancer
- Life and death partners: apoptosis, autophagy and the cross-talk between them
- (2009) A Eisenberg-Lerner et al. CELL DEATH AND DIFFERENTIATION
- Targeting cancer cells by ROS-mediated mechanisms: a radical therapeutic approach?
- (2009) Dunyaporn Trachootham et al. NATURE REVIEWS DRUG DISCOVERY
- Celastrol inhibits the growth of human glioma xenografts in nude mice through suppressing VEGFR expression
- (2008) Yulun Huang et al. CANCER LETTERS
- Apoptosis and non-apoptotic deaths in cancer development and treatment response
- (2008) Elza C. de Bruin et al. CANCER TREATMENT REVIEWS
- Classification of cell death: recommendations of the Nomenclature Committee on Cell Death 2009
- (2008) G Kroemer et al. CELL DEATH AND DIFFERENTIATION
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