Calyxin Y induces hydrogen peroxide-dependent autophagy and apoptosis via JNK activation in human non-small cell lung cancer NCI-H460 cells

Zhang, Chao; Yang, Lei; Wang, Xiaobing; Wang, Junsong; Geng, Yadi; Yang, Changshui

doi:10.1016/j.canlet.2013.06.021

Cited by 70 publications

(61 citation statements)

References 59 publications

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“…Most cancer therapeutic regimens including chemotherapy, inhibit tumors by activating apoptosis (Zhang et al, 2013). In our study, dietary flavonoid, fisetin at concentrations 20-100 µM induced a decrease in the viability of U-2 OS cells.…”

Section: Discussionsupporting

confidence: 48%

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

Huang

et al. 2015

Bangladesh J Pharmacol

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Human osteosarcoma is the most prevalent primary malignant bone tumor with high frequency of invasion and metastasis. Strong resistance coupled with toxicity of the currently available chemotherapeutic drugs poses challenge in treatment. The study aimed to investigate if fisetin, a dietary flavonoid induced apoptosis in human osteosarcoma (U-2 OS) cells. Fisetin at 20-100 µM effectively reduced the viability of OS cells, and induced apoptosis by significantly inducing the expression of caspases (Caspases-3,-8 and -9) and proapoptotic proteins (Bax and Bad) with subsequent down-regulation of Bcl-xL and Bcl-2. While fisetin inhibited PI3K/Akt pathway and ERK1/2, it caused enhanced expressions of p-JNK, p-c-Jun and p-p38. Fisetin-induced ROS generation and decrease in mitochondrial membrane potential would have also contributed to rise in apoptotic cell counts. The observations suggest that fisetin was able to effectively induce apoptosis of U-2 OS cells through ROS generation and modulation of MAPK and PI3K/Akt signalling cascades. Article Info

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Section: Discussionsupporting

confidence: 48%

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

Huang

et al. 2015

Bangladesh J Pharmacol

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“…Zhang et al [30] reported that hydrogen peroxide indicated oxidative stress induced parallel autophagy and apoptosis in human glioma U251 Cells. Kong et al [61] reported that Calyxin Y induces hydrogen peroxide-dependent autophagy in human non-small cell lung cancer NCI-H460 cells. Hence, our demonstration that autophagy in NP cells was induced by H 2 O 2 might not be surprising.…”

Section: Discussionmentioning

confidence: 99%

The Responses of Autophagy and Apoptosis to Oxidative Stress in Nucleus Pulposus Cells: Implications for Disc Degeneration

Chen

et al. 2014

Cell Physiol Biochem

155

126

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Background/Aims: Apoptosis and autophagy are two patterns of programmed cell death which play important roles in the intervertebral disc degeneration. Oxidative stress is an important factor for the induction of programmed cell death. However, the cellular reactions linking autophagy to apoptosis of disc cells under oxidative stress have never been described. This study investigated the responses of autophagy and apoptosis and their interactions in the nucleus pulposus cells (NP cells) under oxidative stress, with the aim to better understand the mechanism of disc degeneration. Methods: NP cells isolated from rat lumbar discs were subjected to different concentrations of H₂O₂ for various time periods. Cell viability was determined by CCK-8 assay, and their apoptosis and autophagy responses were evaluated by fluorescent analysis, flow cytometry and western blotting, et al. The interactions of autophagy and apoptosis and the possible signaling pathways were also investigated by using autophagy modulators. Results: H₂O₂ increased the lysosomal membrane permeability in the NP cells and induced apoptosis through the mitochondrial pathway subsequently. Meanwhile, H₂O₂ stimulated an early autophagy response through the ERK/m-TOR signaling pathway. Autophagy inhibition significantly decreased the apoptosis incidence in the cells insulted by H₂O₂. Conclusion: These results suggested that controlling the autophagy response in the NP cells under oxidative stress should be beneficial for the survival of the cells and probably delay the process of disc degeneration.

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“…The cross talk between autophagy and apoptosis in tumor is complex [46]. On one hand, apoptotic signaling triggers protective autophagy to occur; on the other hand, excessive autophagy may digest the cellular organelles beyond a certain threshold, causing irreversible collapse of vital functions in cells, since the volume occupied by autophagic vacuoles may be roughly equal to the free cytosol and organelles during autophagy [47e49].…”

Section: Protective Autophagy In the Agnps Associated-radiotherapymentioning

confidence: 99%

Is the autophagy a friend or foe in the silver nanoparticles associated radiotherapy for glioma？

Wu¹,

Lin²,

Liu³

et al. 2015

Biomaterials

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Calyxin Y induces hydrogen peroxide-dependent autophagy and apoptosis via JNK activation in human non-small cell lung cancer NCI-H460 cells

Cited by 70 publications

References 59 publications

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

Fisetin, a dietary flavonoid induces apoptosis via modulating the MAPK and PI3K/Akt signalling pathways in human osteosarcoma (U-2 OS) cells

The Responses of Autophagy and Apoptosis to Oxidative Stress in Nucleus Pulposus Cells: Implications for Disc Degeneration

Is the autophagy a friend or foe in the silver nanoparticles associated radiotherapy for glioma？

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