β-elemene regulates endoplasmic reticulum stress to induce the apoptosis of NSCLC cells through PERK/IRE1α/ATF6 pathway

Liu, Ying; Jiang, Ziyu; Zhou, Yufang; Qiu, Huihui; Wang, Gang; Luo, Yi; Liu, Jing-bing; Liu, Xiongwei; Bu, Weiquan; Song, Jie; Cui, Li; Jia, Xiao‐Bin; Feng, Liang

doi:10.1016/j.biopha.2017.06.073

Cited by 53 publications

(36 citation statements)

References 26 publications

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“…Importantly, the combination of β‐elemene and TRAIL induced DR5, Caspase‐8 and FADD translocation into lipid rafts, and the cleavage of Caspase‐8 was also detected (1 and 2, Figure B). In addition, β‐elemene was reported to induce the apoptosis of lung cancer A549 cells through PERK/IRE1a/ATF6 pathway (Liu et al, ). In our study, β‐elemene alone also induced the upregulation of PERK, IRE1a and ATF6 in gastric cancer cells.…”

Section: Resultsmentioning

confidence: 99%

“…However, nystatin partially prevented the localization of DR5 clustering in lipid rafts and DISC formation, and followed apoptosis induced by β‐elemene combined with TRAIL. In addition, β‐elemene has been reported to regulate endoplasmic reticulum stress to trigger apoptosis by PERK/IRE1α/ATF6 pathway in lung cancer cells (Liu et al, ). In the present study, β‐elemene alone upregulated the expression of PERK, IRE1a and ATF6 in gastric cancer cells.…”

Section: Discussionmentioning

confidence: 99%

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β‐elemene increases the sensitivity of gastric cancer cells to TRAIL by promoting the formation of DISC in lipid rafts

Guo

et al. 2018

Cell Biology International

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β-Elemene, an anti-cancer drug extracted from traditional Chinese medicinal herb, showed anti-tumor effects on gastric cancer cells. Our previous studies reported gastric cancer cells are insensitive to TRAIL. However, whether β-elemene could enhance anti-cancer effects of TRAIL on gastric cancer cells is unknown. In our present study, β-elemene prevented gastric cancer cell viability in dose-dependent manner, and when combined with TRAIL, obviously inhibited proliferation and promoted apoptosis in gastric cancer cells. Compared to β-elemene or TRAIL alone, treatment with β-elemene and TRAIL obviously promoted DR5 clustering as well as translocation of Caspase-8, DR5 and FADD into lipid rafts. This led to cleavage of Caspase-8 and the formation of death-inducing signaling complex (DISC) in lipid rafts. The cholesterol-sequestering agent nystatin partially reversed DR5 clustering and DISC formation, preventing apoptosis triggered by the combination of β-elemene and TRAIL. Our results suggest that β-elemene increases the sensitivity of gastric cancer cells to TRAIL partially by promoting the formation of DISC in lipid rafts.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

β‐elemene increases the sensitivity of gastric cancer cells to TRAIL by promoting the formation of DISC in lipid rafts

Guo

et al. 2018

Cell Biology International

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“…Karmakar and collaborators demonstrated that curcumin induces apoptosis in human glioblastoma T98G cells by activating both receptor-mediated and mitochondria-mediated proteolytic pathways (Karmakar, Banik, Patel, & Ray, 2006). Wang et al (2017) found that curcumin treatment inhibits cell growth, induces apoptosis and suppress migration and invasion by reducing the expression of cancer signaling pathways (i.e., Notch1 and pAKT) and of neuronal precursor cell-expressed developmentally downregulated 4-1 (NEDD4) protein in human glioma cells. Mukherjee et al (2016) demonstrated that the delivery of a glioblastoma-directed adduct of curcumin into the brain of GBM mice caused tumor remission in 50% of the animals (Mukherjee et al, 2016).…”

Section: Several In Vitro and In Vivo Experiments Have Demonstrated Tmentioning

confidence: 99%

Adult‐onset brain tumors and neurodegeneration: Are polyphenols protective?

Squillaro

Schettino

Sampaolo

et al. 2017

Journal Cellular Physiology

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Aging is a primary risk factor for both neurodegenerative disorders (NDs) and tumors such as adult-onset brain tumors. Since NDs and tumors are severe, disabling, progressive and often incurable conditions, they represent a pressing problem in terms of human suffering and economic costs to the healthcare systems. The current challenge for physicians and researchers is to develop new therapeutic strategies in both areas to improve the patients' quality of life. In addition to genetics and environmental stressors, the increase in cellular oxidative stress as one of the potential common etiologies has been reported for both disorders. Recently, the scientific community has focused on the beneficial effects of dietary antioxidant classes, known as nutraceuticals, such as carotenoids, vitamins, and polyphenols. Among these compounds, polyphenols are considered to be one of the most bioactive agents in neurodegeneration and tumor prevention. Despite the beneficial activity of polyphenols, their poor bioavailability and inefficient delivery systems are the main factors limiting their use in medicine and functional food. The development of polymeric nanoparticle-based delivery systems able to encapsulate and preserve polyphenolic compounds may represent a promising tool to enhance their stability, solubility, and cell membrane permeation. In the present review we provide an overview of the main polyphenolic compounds used for ND and brain tumor prevention and treatment that explores their mechanisms of action, recent clinical findings and principal factors limiting their application in medicine.

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“…β‐Elemene can be isolated from the Curcuma wenyujin plant and has been widely used in China for the treatment of various cancer types (Y. Liu et al, ; Zhai et al, ; G. N. Zhang, Ashby, Zhang, Chen, & Guo, ). Several studies have revealed that β‐elemene can inhibit cell proliferation and induce apoptosis in a variety of cancers, including breast (B. Zhang, Zhang, Tang, Zheng, & Zhang, ) and lung cancers (J. Liu et al, ; Y. Liu et al, ). Recent studies have demonstrated that β‐elemene can reduce B16F10 melanoma cell invasion (Shi et al, ) and reduce the metastatic potential of MCF‐7 breast cancer cells (X. Zhang, Zhang, & Li, ).…”

Section: Introductionmentioning

confidence: 99%

“…β-Elemene can be isolated from the Curcuma wenyujin plant and has been widely used in China for the treatment of various cancer types (Y. Liu et al, 2017;Zhai et al, 2018;G. N. Zhang, Ashby, Zhang, Chen, & Guo, 2015).…”

Section: Introductionmentioning

confidence: 99%

β‐Elemene inhibits peritoneal metastasis of gastric cancer cells by modulating FAK/Claudin‐1 signaling

Deng

Zhang

Liu

et al. 2019

Phytotherapy Research

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Peritoneal metastasis is common in advanced gastric cancer patients and is typically associated with a worse prognosis. β‐Elemene is a natural compound that can be isolated from the Curcuma wenyujin plant and has been widely used in China to treat a variety of cancers. However, the anti‐metastatic impacts of β‐elemene on gastric cancer remain unknown. In our study, we found that β‐elemene significantly inhibited the migration and invasive capacity of gastric cells in vitro and inhibited the capacity of gastric cancer cells to peritoneally diffuse and metastasize in vivo. Mechanistically, we demonstrated that the anti‐metastatic effects of β‐elemene were exerted by downregulating the expression of Claudin‐1. Furthermore, β‐elemene was found to inhibit the metastatic capacity of cells by downregulating FAK phosphorylation, which regulated Claudin‐1. Overall, our result revealed that β‐elemene inhibited peritoneal metastases from gastric cancer by modulating the FAK/Claudin‐1 pathway.

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β-elemene regulates endoplasmic reticulum stress to induce the apoptosis of NSCLC cells through PERK/IRE1α/ATF6 pathway

Cited by 53 publications

References 26 publications

β‐elemene increases the sensitivity of gastric cancer cells to TRAIL by promoting the formation of DISC in lipid rafts

β‐elemene increases the sensitivity of gastric cancer cells to TRAIL by promoting the formation of DISC in lipid rafts

Adult‐onset brain tumors and neurodegeneration: Are polyphenols protective?

β‐Elemene inhibits peritoneal metastasis of gastric cancer cells by modulating FAK/Claudin‐1 signaling

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