scholarly journals ABT-737 potentiates cisplatin-induced apoptosis in human osteosarcoma cells via the mitochondrial apoptotic pathway

2017 ◽  
Vol 38 (4) ◽  
pp. 2301-2308 ◽  
Author(s):  
Fengtian Zhang ◽  
Xiaolong Yu ◽  
Xuqiang Liu ◽  
Tonghua Zhou ◽  
Tao Nie ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis

scholarly journals CLEFMA Activates the Extrinsic and Intrinsic Apoptotic Processes through JNK1/2 and p38 Pathways in Human Osteosarcoma Cells

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3280 ◽  
Author(s):  
Jia-Sin Yang ◽  
Renn-Chia Lin ◽  
Yi-Hsien Hsieh ◽  
Heng-Hsiung Wu ◽  
Geng-Chung Li ◽  
...  
Keyword(s):  
Annexin V ◽  
Synthetic Analog ◽  
Osteosarcoma Cells ◽  
Apoptotic Pathway ◽  
Term Survival ◽  
Anticancer Properties ◽  
Human Osteosarcoma ◽  
Effector Caspase ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis

Due to the poor prognosis of metastatic osteosarcoma, chemotherapy is usually employed in the adjuvant situation to improve the prognosis and the chances of long-term survival. 4-[3,5-Bis(2-chlorobenzylidene)-4-oxo-piperidine-1-yl]-4-oxo-2-butenoic acid (CLEFMA) is a synthetic analog of curcumin and possesses anti-inflammatory and anticancer properties. To further obtain information regarding the apoptotic pathway induced by CLEFMA in osteosarcoma cells, microculture tetrazolium assay, annexin V-FITC/PI apoptosis staining assay, human apoptosis array, and Western blotting were employed. CLEFMA dose-dependently decreased the cell viabilities of human osteosarcoma U2OS and HOS cells and significantly induced apoptosis in human osteosarcoma cells. In addition to the effector caspase 3, CLEFMA significantly activated both extrinsic caspase 8 and intrinsic caspase 9 initiators. Moreover, CLEFMA increased the phosphorylation of extracellular signal-regulated protein kinases (ERK)1/2, c-Jun N-terminal kinases (JNK)1/2 and p38. Using inhibitors of JNK (JNK-in-8) and p38 (SB203580), CLEFMA’s increases of cleaved caspases 3, 8, and 9 could be expectedly suppressed, but they could not be affected by co-treatment with the ERK inhibitor (U0126). Conclusively, CLEFMA activates both extrinsic and intrinsic apoptotic pathways in human osteosarcoma cells through JNK and p38 signaling. These findings contribute to a better understanding of the mechanisms responsible for CLEFMA’s apoptotic effects on human osteosarcoma cells.

scholarly journals Celastrol induces apoptosis of human osteosarcoma cells via the mitochondrial apoptotic pathway

2015 ◽  
Vol 34 (3) ◽  
pp. 1129-1136 ◽  
Author(s):  
XIAOLONG YU ◽  
XIN ZHOU ◽  
CHANGLIN FU ◽  
QIANG WANG ◽  
TAO NIE ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Apoptotic Pathway ◽  
Mitochondrial Apoptotic Pathway ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells

Autophagy Inhibition Promotes Quercetin Induced Apoptosis in MG-63 Human Osteosarcoma cells

2015 ◽  
Vol 40 (2) ◽  
pp. 85-91 ◽  
Author(s):  
Sung-Jin Park ◽  
◽  
Su-Bin Yu ◽  
Yong-Ho Kim ◽  
In-Ryoung Kim ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis ◽  
Autophagy Inhibition

scholarly journals p14ARF sensitizes human osteosarcoma cells to cisplatin-induced apoptosis in a p53-independent manner

2007 ◽  
Vol 6 (7) ◽  
pp. 1074-1080 ◽  
Author(s):  
Xiang-Wei Yuan ◽  
Xiao-Feng Zhu ◽  
Xiu-Fang Huang ◽  
Pu-Yi Sheng ◽  
Ai-Shan He ◽  
...  
Keyword(s):  
Osteosarcoma Cells ◽  
Independent Manner ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Induced Apoptosis

Neohesperidin Induces Cell Cycle Arrest, Apoptosis, and Autophagy via the ROS/JNK Signaling Pathway in Human Osteosarcoma Cells

2021 ◽  
pp. 1-24
Author(s):  
Shubin Wang ◽  
Zongguang Li ◽  
Wei Liu ◽  
Guojun Wei ◽  
Naichun Yu ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Signaling Pathway ◽  
Osteosarcoma Cell ◽  
Osteosarcoma Cells ◽  
Jnk Signaling ◽  
Human Osteosarcoma ◽  
Human Osteosarcoma Cells ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis

Neohesperidin has anti-oxidative and anti-inflammatory properties and exerts extensive therapeutic effects on various cancers. In this study, the osteosarcoma cell lines were exposed to different concentrations of neohesperidin. Cell proliferation and viability were assessed by CCK-8 and colony-formation assays. The role of neohesperidin in cell cycle progression and apoptosis were analyzed by flow cytometry and western blotting. To identify autophagosomes and autolysosomes, we used a tandem GFP-mRFP-LC3B lentiviral construct. In addition, autophagy was evaluated by examining autophagosome formation using transmission electron microscopy. Intracellular reactive oxygen species (ROS) production was detected by fluorescence microscopy and flow cytometry. Subsequently, the activation of the ROS/JNK signaling pathway was investigated. Neohesperidin could inhibit proliferation and induce apoptosis in SJSA and HOS cells. The formation of autophagosomes indicated that autophagy occurred in neohesperidin-treated cells and the apoptotic effect of neohesperidin was significantly increased after the use of autophagy inhibitors. Subsequently, we found that neohesperidin-induced apoptosis and autophagy were related to the increase in ROS generation and were significantly inhibited by GSH. Moreover, neohesperidin induced activation of the c-Jun N-terminal kinase (JNK) signaling pathway and inhibition of JNK with SP600125 attenuated neohesperidin-induced apoptosis and autophagy simultaneously. Our data indicated that neohesperidin caused G2/M phase arrest and induced apoptosis and autophagy by activating the ROS/JNK pathway in human osteosarcoma cells, suggesting that neohesperidin is a potential drug candidate for the treatment of osteosarcomas.

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