Nanosized Titanium Dioxide Induced Apoptosis and Abnormal Expression of Blood-Testis Barrier Junction Proteins Through JNK Signaling Pathway in TM4 Cells

Eleven notoamides including four new congeners were isolated fromAspergillus ochraceus. Notoamide G inhibited the viability of hepatocellular carcinoma cell lines by regulation of apoptosis and autophagy through P38/JNK signaling pathway.

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Silencing of Gal-7 inhibits TGF-β1-induced apoptosis of human airway epithelial cells through JNK signaling pathway

Experimental Cell Research ◽

10.1016/j.yexcr.2018.12.017 ◽

2019 ◽

Vol 375 (2) ◽

pp. 100-105 ◽

Cited By ~ 4

Author(s):

Xinrong Sun ◽

Wanggang Zhang

Keyword(s):

Epithelial Cells ◽

Signaling Pathway ◽

Airway Epithelial Cells ◽

Airway Epithelial ◽

Jnk Signaling ◽

Human Airway ◽

Jnk Signaling Pathway ◽

Induced Apoptosis ◽

Tgf Β1 ◽

Human Airway Epithelial Cells

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Propranolol induced apoptosis and autophagy via the ROS/JNK signaling pathway in human ovarian cancer

10.21203/rs.3.rs-20682/v1 ◽

2020 ◽

Author(s):

Shujun Zhao ◽

Suzhen Fan ◽

Yanyu Shi ◽

Hongyan Ren ◽

Hanqing Hong ◽

...

Keyword(s):

Ovarian Cancer ◽

Flow Cytometry ◽

Signaling Pathway ◽

Cell Apoptosis ◽

Human Ovarian Cancer ◽

Dependent Manner ◽

Flow Cytometry Analysis ◽

Jnk Signaling ◽

Jnk Signaling Pathway ◽

Induced Apoptosis

Abstract Background: Propranolol has a significant anti-cancer effect on various cancers. The present study aimed to investigate the underlying mechanism behind the therapeutic effect of Propranolol on the ovarian cancer.Materials and methods: The effect of Propranolol on cell viability was examined by MTT analysis. Cellular apoptosis was evaluated by flow cytometry analysis. Autophagy was defined by autophagosome observed by confocal microscopy after infected with GFP-LC3 adenovirus. In addition, the expression of marker proteins involved in cell apoptosis, autophagy, and ROS/JNK signaling pathway were estimated by Western Blotting assay.Results: Propranolol significantly reduced the viability of human ovarian cancer cell lines SKOV-3 and A2780 in a dose- and time-dependent manner. Flow cytometry analysis revealed that Propranolol induced the cell cycle arrest at G2/M phase and resulted in apoptosis. Moreover, autophagy inhibitor 3-MA markedly enhanced the Propranolol-induced apoptosis. In addition, reactive oxygen species (ROS) was demonstrated dramatically increased after Propranolol treatment and Propranolol activated the phosphorylation of JNK. What is more, p38 inhibitor SB203580 and JNK inhibitor SP600125 attenuated the upregulated expression of LC3-II and cleaved-caspase-3 by the effect of Propranolol. ROS exclusive inhibitor antioxidant N-acetyl cysteine (NAC) weaken the phosphorylation of JNK proteins induced by Propranolol.Conclusions：In summary, our results suggested that Propranolol induced cell apoptosis and protective autophagy through the ROS/JNK signaling pathway in human ovarian cancer cells.

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

The American Journal of Chinese Medicine ◽

10.1142/s0192415x21500609 ◽

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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