The Mechanism of NPC-14686-Induced [Ca^(2+)]i Rises and Non-Ca^(2+)-Triggered Cell Death in MG63 Human Osteosarcoma Cells

2014 ◽  
Vol 57 (3) ◽  
pp. 158-166 ◽  
Author(s):  
Jau-Min Chien
Keyword(s):  
Cell Death ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Ketoconazole-induced JNK phosphorylation and subsequent cell death via apoptosis in human osteosarcoma cells

2009 ◽  
Vol 23 (7) ◽  
pp. 1268-1276 ◽  
Author(s):  
Ko-Long Lin ◽  
Chorng-Chih Huang ◽  
Jin-Shiung Cheng ◽  
Jeng-Yu Tsai ◽  
Yih-Chau Lu ◽  
...  
Keyword(s):  
Cell Death ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

scholarly journals Decoding the anticancer activity of VO-clioquinol compound: the mechanism of action and cell death pathways in human osteosarcoma cells

Metallomics ◽  
2017 ◽  
Vol 9 (7) ◽  
pp. 891-901 ◽  
Author(s):  
Ignacio E. León ◽  
Paula Díez ◽  
Enrique J. Baran ◽  
Susana B. Etcheverry ◽  
Manuel Fuentes
Keyword(s):  
Cell Death ◽  
Anticancer Drugs ◽  
Mechanism Of Action ◽  
Platinum Metal ◽  
Osteosarcoma Cells ◽  
Vanadium Compounds ◽  
New Class ◽  
Human Osteosarcoma ◽  
Cell Death Pathways ◽  
Human Osteosarcoma Cells

Vanadium compounds were studied in recent years by considering them as a representative of a new class of non-platinum metal anticancer drugs.

scholarly journals The plant alkaloid voacamine induces apoptosis-independent autophagic cell death on both sensitive and multidrug resistant human osteosarcoma cells

Autophagy ◽  
2008 ◽  
Vol 4 (8) ◽  
pp. 1020-1033 ◽  
Author(s):  
Stefania Meschini ◽  
Maria Condello ◽  
Annarica Calcabrini ◽  
Manuela Marra ◽  
Giuseppe Formisano ◽  
...  
Keyword(s):  
Cell Death ◽  
Multidrug Resistant ◽  
Autophagic Cell Death ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Hyperthermia enhances the effect of β-lapachone to cause γH2AX formations and cell death in human osteosarcoma cells

2010 ◽  
Vol 27 (1) ◽  
pp. 53-62 ◽  
Author(s):  
Takeshi Hori ◽  
Takashi Kondo ◽  
Hyemi Lee ◽  
Chang W. Song ◽  
Heon Joo Park
Keyword(s):  
Cell Death ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Anandamide-induced Ca2+ elevation leading to p38 MAPK phosphorylation and subsequent cell death via apoptosis in human osteosarcoma cells

Toxicology ◽  
2007 ◽  
Vol 231 (1) ◽  
pp. 21-29 ◽  
Author(s):  
Shu-Shong Hsu ◽  
Chun-Jen Huang ◽  
He-Hsiung Cheng ◽  
Chiang-Ting Chou ◽  
Hsiao-Ying Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
P38 Mapk ◽  
Osteosarcoma Cells ◽  
Mapk Phosphorylation ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

scholarly journals β-Phenethyl Isothiocyanate Induces Cell Death in Human Osteosarcoma through Altering Iron Metabolism, Disturbing the Redox Balance, and Activating the MAPK Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-23
Author(s):  
Huanhuan Lv ◽  
Chenxiao Zhen ◽  
Junyu Liu ◽  
Peng Shang
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Iron Metabolism ◽  
Ros Generation ◽  
Osteosarcoma Cell ◽  
Phenethyl Isothiocyanate ◽  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Human Osteosarcoma Cell

Osteosarcoma is the most common primary malignancy of the skeleton in children and adults. The outcomes of people with osteosarcomas are unsatisfied. β-Phenethyl isothiocyanate (PEITC) exhibits chemoprevention and chemotherapeutic activities against many human cancers. The molecular mechanism underlying its action on osteosarcoma is still unknown. This study was aimed at investigating the effect of PEITC on human osteosarcoma both in vitro and in vivo. The results showed that PEITC reduced cell viability, inhibited proliferation, and caused G2/M cell cycle arrest in four human osteosarcoma cell lines (MNNG/HOS, U-2 OS, MG-63, and 143B). Then, we found that PEITC altered iron metabolism related to the processes of iron import, storage, and export, which resulted in increased labile iron. Expectedly, PEITC caused oxidative stress as a consequence of GSH depletion-inducing ROS generation and lipid peroxidation. Multiple cell death modalities, including ferroptosis, apoptosis, and autophagy, were triggered in human osteosarcoma cells. Three MAPKs (ERK, p38, and JNK) were all activated after PEITC treatment; however, they presented different responses among the four human osteosarcoma cell lines. ROS generation was proved to be the major cause of PEITC-induced decreased proliferative potential, altered iron metabolism, cell death, and activated MAPKs in human osteosarcoma cells. In addition, PEITC also significantly delayed tumor growth in a xenograft osteosarcoma mouse model with a 30 mg/kg administration dose. In conclusion, this study reveals that PEITC simultaneously triggers ferroptosis, apoptosis, and autophagy in human osteosarcoma cells by inducing oxidative stress.

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