Inhibition of autophagy by 3-methyladenine potentiates sulforaphane-induced cell death of BE(2)-C human neuroblastoma cells

Horwacik, Irena; Gaik, Monika; Durbas, Małgorzata; Boratyn, Elżbieta; Zając, Grzegorz; Szychowska, Katarzyna; Szczodrak, Małgorzata; Kołoczek, Henryk; Rokita, Hanna

doi:10.3892/mmr.2015.3377

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…Moreover, CQ potentiated the cytotoxicity of topotecan in lung cancer cells by interfering with autophagy , and the antitumor efficiency of cucurbitacin I is promoted with synergetic treatment of CQ in glioblastoma . Additionally, cell death of BE (2)-C human neuroblastoma cells following sulforaphane treatment could be promoted by 3-MA via inhibition of autophagy (Horwacik et al, 2015). Honokiol is isolated from the bark, seed cones, and leaves of trees belonging to the genus Magnolia and is a kind of lignan.…”

Section: Natural Compoundsmentioning

confidence: 99%

Combination of an Autophagy Inducer and an Autophagy Inhibitor: A Smarter Strategy Emerging in Cancer Therapy

Liu

Zhang

et al. 2020

Front. Pharmacol.

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Autophagy is considered a cytoprotective function in cancer therapy under certain conditions and is a drug resistance mechanism that represents a clinical obstacle to successful cancer treatment and leads to poor prognosis in cancer patients. Because certain clinical drugs and agents in development have cytoprotective autophagy effects, targeting autophagic pathways has emerged as a potential smarter strategy for cancer therapy. Multiple preclinical and clinical studies have demonstrated that autophagy inhibition augments the efficacy of anticancer agents in various cancers. Autophagy inhibitors, such as chloroquine and hydroxychloroquine, have already been clinically approved, promoting drug combination treatment by targeting autophagic pathways as a means of discovering and developing more novel and more effective cancer therapeutic approaches. We summarize current studies that focus on the antitumor efficiency of agents that induce cytoprotective autophagy combined with autophagy inhibitors. Furthermore, we discuss the challenge and development of targeting cytoprotective autophagy as a cancer therapeutic approach in clinical application. Thus, we need to facilitate the exploitation of appropriate autophagy inhibitors and coadministration delivery system to cooperate with anticancer drugs. This review aims to note optimal combination strategies by modulating autophagy for therapeutic advantage to overcome drug resistance and enhance the effect of antitumor therapies on cancer patients.

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Section: Natural Compoundsmentioning

confidence: 99%

Combination of an Autophagy Inducer and an Autophagy Inhibitor: A Smarter Strategy Emerging in Cancer Therapy

Liu

Zhang

et al. 2020

Front. Pharmacol.

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“…ITCs can act as autophagic inducers and, by doing so, they may exert either a protective role [148,149,150,151,152,153,154,155,156,157] or promote cell death [158,159,160,161,162] according to tumour type, stage and genetic context. To this end, a recent study investigated the autophagic involvement on BITC-induced inhibition of cell growth in lung cancer cells and showed an induction of ER (endoplasmatic reticulum) stress-mediated autophagy capable of protecting from the suppressive effects of BITC on cancer cell growth.…”

Section: Introductionmentioning

confidence: 99%

The Role of Isothiocyanates as Cancer Chemo-Preventive, Chemo-Therapeutic and Anti-Melanoma Agents

et al. 2019

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Many studies have shown evidence in support of the beneficial effects of phytochemicals in preventing chronic diseases, including cancer. Among such phytochemicals, sulphur-containing compounds (e.g., isothiocyanates (ITCs)) have raised scientific interest by exerting unique chemo-preventive properties against cancer pathogenesis. ITCs are the major biologically active compounds capable of mediating the anticancer effect of cruciferous vegetables. Recently, many studies have shown that a higher intake of cruciferous vegetables is associated with reduced risk of developing various forms of cancers primarily due to a plurality of effects, including (i) metabolic activation and detoxification, (ii) inflammation, (iii) angiogenesis, (iv) metastasis and (v) regulation of the epigenetic machinery. In the context of human malignant melanoma, a number of studies suggest that ITCs can cause cell cycle growth arrest and also induce apoptosis in human malignant melanoma cells. On such basis, ITCs could serve as promising chemo-therapeutic agents that could be used in the clinical setting to potentiate the efficacy of existing therapies.

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“…Autophagy can participate in a number of pathological processes and influence the prognosis of the diseases [ 9 , 47 – 50 ]. In our study, we used 3-MA, a widely used autophagy inhibitor [ 51 ], to explore the effect of autophagy in ALI. We evaluated autophagy by detecting autophagy sensitive indices: LCII, autophagosome by electron microscopy, and p62 [ 52 – 54 ].…”

Section: Discussionmentioning

confidence: 99%

The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice

Gao

Wang

et al. 2018

Med Sci Monit

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BackgroundAcute lung injury (ALI) is responsible for mortality in hospitalized patients. Autophagy can negatively regulate inflammatory response, and CXCL16 (chemokine (C-X-C motif) ligand 16) is a kind of chemokine, which is closely related to the inflammatory response. However, the relationship between autophagy and CXCL16 in ALI is still unclear. This study aimed to investigate the role of autophagy and chemokine CXCL16 in ALI in mice.Material/MethodsThirty-two male C57BL/6 mice were divided into four groups. The control group (C group) was given normal saline through intraperitoneal injection. The L group was given LPS (lipopolysaccharide) at 30 mg/kg to construct an ALI model. The 3-MA group received an intraperitoneal injection of inhibitor of autophagy 3-methyladenine at 15 mg/kg, 30 minutes before LPS injection. The anti-CXCL16 group was given 20 mg/kg of CXCL16 monoclonal antibody 30 minutes before the LPS injection.ResultsIn the 3-MA Group, the level of histological analysis, lung wet/dry ratio, total protein of BAL (bronchoalveolar lavage fluid) and TNF-α level were higher than the L group (p<0.05), the level of autophagy was lower than the L group (p<0.05), and the level of CXCL16 was higher than the L group (p<0.05). In the anti-CXCL16 group, the level of histological analysis, lung wet/dry ratio, BAL protein, and TNF-α level were declined compared to the L group (p<0.05), but there was no statistically significant difference in expression of CXCL16 detected by ELISA between the anti-CXCL16 group and the L group (p>0.05).ConclusionsAutophagy played a protective role in ALI induced by LPS in mice. Autophagy could regulate the level of CXCL16. The chemokine CXCL16 could exacerbate ALI.

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Inhibition of autophagy by 3-methyladenine potentiates sulforaphane-induced cell death of BE(2)-C human neuroblastoma cells

Cited by 14 publications

References 25 publications

Combination of an Autophagy Inducer and an Autophagy Inhibitor: A Smarter Strategy Emerging in Cancer Therapy

Combination of an Autophagy Inducer and an Autophagy Inhibitor: A Smarter Strategy Emerging in Cancer Therapy

The Role of Isothiocyanates as Cancer Chemo-Preventive, Chemo-Therapeutic and Anti-Melanoma Agents

The Role of Autophagy and the Chemokine (C-X-C Motif) Ligand 16 During Acute Lung Injury in Mice

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