Sulforaphane Induced Apoptosis via Promotion of Mitochondrial Fusion and ERK1/2-Mediated 26S Proteasome Degradation of Novel Pro-survival Bim and Upregulation of Bax in Human Non-Small Cell Lung Cancer Cells

Yang, Geng; Zhou, Yan; Wu, Shuqi; Hu, Yongbin; Lin, Kai; Wang, Yalin; Zheng, Zhongnan; Wu, Wei

doi:10.7150/jca.19383

Cited by 40 publications

(33 citation statements)

References 33 publications

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“…The present study is the first to illustrate that inhibition of esophageal cancer cells using a CXCL antagonist may occur via inhibition of the PI3K/AKT signaling pathway. Previous studies have indicated that cell proliferation is strongly associated with cell apoptosis in the development of numerous types of cancer (31)(32)(33)(34)(35). In the present study, a reduction in cell proliferation was accompanied by increased apoptosis following treatment with UNBS5162, as determined by CCK-8 assays, flow cytometry and alterations in the expression of apoptosis-associated proteins.…”

Section: Discussionsupporting

confidence: 68%

UNBS5162 inhibits the proliferation of esophageal cancer squamous cells via the PI3K/AKT signaling pathway

Zhang

2017

Mol Med Report

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C‑X‑C motif chemokine ligand (CXCL) signaling has been demonstrated to be involved in cancer invasion and migration; therefore, CXCL antagonists may serve as anticancer drugs by preventing tumor proliferation. The present study aimed to investigate whether a pan antagonist of CXCLs, UNBS5162, may inhibit esophageal cancer proliferation and to identify the underlying mechanisms. Cell proliferation and cell colony formation results, which were determined by a Cell Counting Kit‑8 assay and crystal violet staining, respectively, demonstrated that UNBS5162 inhibited esophageal cancer cell proliferation. Following treatment with UNBS5162, Transwell migration and Matrigel invasion assays, and flow cytometry with Annexin V‑fluorescein isothiocyanate and propidium iodide staining, were performed to investigate cell migration, invasion and apoptosis in human esophageal cancer cells. The results indicated that invasion and migration was reduced in UNBS5162‑treated cells, while apoptosis was increased. Western blotting experiments confirmed that UNBS5162 downregulated the protein expression of proteins associated with the phosphatidylinositol 3‑kinase (PI3K)/AKT signaling pathway, including the levels of phosphorylated (p)‑AKT, p‑mechanistic target of rapamycin kinase, ribosomal protein S6 kinase β1 and cyclin D1. In addition, upregulated expression of programed cell death 4 was observed following UNBS5162 treatment. The present study demonstrated that UNBS5162 is a novel naphthalimide that may have potential therapeutic use for the prevention of esophageal cancer proliferation and metastasis via the PI3K/AKT signaling pathway.

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Section: Discussionsupporting

confidence: 68%

UNBS5162 inhibits the proliferation of esophageal cancer squamous cells via the PI3K/AKT signaling pathway

Zhang

2017

Mol Med Report

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“…ERK1/2 MAPK pathway is activated by different stimulus including growing factors, mechanical stress and so on (36). The activation of ERK1/2 is necessary for signal transduction, from cell membrane surface receptors to nucleus.…”

Section: Discussionmentioning

confidence: 99%

Lycium�barbarum polysaccharides attenuates the apoptosis of hippocampal neurons induced by sevoflurane

Xie

Wang

2018

Exp Ther Med

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Following the application of inhalational anesthetics, including sevoflurane, patients may suffer from neural injury. The present study was conducted to explore the mechanism involved in Lycium barbarum polysaccharides (LBP) treatment of sevoflurane injured hippocampal neurons. Primary hippocampal neurons were isolated from Sprague Dawley embryonic rats. The Cell Counting Kit-8 (CCK-8) assay was used to detect cell viability. Furthermore, flow cytometry (FCM) was used to determine cell proliferation and apoptosis rates. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were applied to detect the expression levels of apoptosis-related factors, including activated-Caspase-3, B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-2 associated X (Bax), phosphorylated extracellular signal-regulated kinase 1/2 (p-ERK1/2) and total ERK1/2. The results showed that LBP promoted cell viability and cell proliferation but inhibited cell apoptosis in neurons injured with 3% sevoflurane, in dose-dependent manners (100, 200 and 400 µg/ml). LBP increased the expression levels of Bcl-2 and p-ERK1/2, and decreased levels of activated-Caspase-3 and Bax in a dose-dependent manner in hippocampal neurons that were injured with sevoflurane. In addition, ERK1/2 inhibitor reversed the above phenomenon in 400 µg/ml LBP and 3% sevoflurane-treated hippocampal neurons. Therefore, the present study indicated that LBP protected hippocampal neurons from sevoflurane injury, including aberrant cell apoptosis, via the ERK1/2 pathway.

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“…Apoptosis can be induced by death receptor 5, activator protein 1, MAP kinases, or mithocondrial dysfunction, or by suppressing the mechanisms responsible for cellular survival, for example, inhibiting activation of the nuclear factor-kappa B [8,9]. Since sulforaphane has these multiple anticancer mechanisms, it is able to inhibit one or more pathways that contribute to malignant transformation and possesses cancer-preventive properties against different tumor diseases [10][11][12], including melanoma [13].…”

Section: Introductionmentioning

confidence: 99%

Sulforaphane-Loaded Ultradeformable Vesicles as A Potential Natural Nanomedicine for the Treatment of Skin Cancer Diseases

et al. 2019

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Sulforaphane is a multi-action drug and its anticancer activity is the reason for the continuous growth of attention being paid to this drug. Sulforaphane shows an in vitro antiproliferative activity against melanoma and other skin cancer diseases. Unfortunately, this natural compound cannot be applied in free form on the skin due to its poor percutaneous permeation determined by its physico-chemical characteristics. The aim of this investigation was to evaluate ethosomes® and transfersomes® as ultradeformable vesicular carriers for the percutaneous delivery of sulforaphane to be used for the treatment of skin cancer diseases. The physico-chemical features of the ultradeformable vesicles were evaluated. Namely, ethosomes® and transfersomes® had mean sizes <400 nm and a polydispersity index close to 0. The stability studies demonstrated that the most suitable ultradeformable vesicles to be used as topical carriers of sulforaphane were ethosomes® made up of ethanol 40% (w/v) and phospholipon 90G 2% (w/v). In particular, in vitro studies of percutaneous permeation through human stratum corneum and epidermis membranes showed an increase of the percutaneous permeation of sulforaphane. The antiproliferative activity of sulforaphane-loaded ethosomes® was tested on SK-MEL 28 and improved anticancer activity was observed in comparison with the free drug.

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Sulforaphane Induced Apoptosis via Promotion of Mitochondrial Fusion and ERK1/2-Mediated 26S Proteasome Degradation of Novel Pro-survival Bim and Upregulation of Bax in Human Non-Small Cell Lung Cancer Cells

Cited by 40 publications

References 33 publications

UNBS5162 inhibits the proliferation of esophageal cancer squamous cells via the PI3K/AKT signaling pathway

UNBS5162 inhibits the proliferation of esophageal cancer squamous cells via the PI3K/AKT signaling pathway

Lycium�barbarum polysaccharides attenuates the apoptosis of hippocampal neurons induced by sevoflurane

Sulforaphane-Loaded Ultradeformable Vesicles as A Potential Natural Nanomedicine for the Treatment of Skin Cancer Diseases

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