Sanguinarine induces apoptosis of human osteosarcoma cells through the extrinsic and intrinsic pathways

Park, Hyunjin; Bergeron, Éric; Senta, Helena; Guillemette, Kim; Beauvais, Sabrina; Blouin, Richard; Sirois, Joël; Faucheux, Nathalie

doi:10.1016/j.bbrc.2010.07.114

Cited by 50 publications

(33 citation statements)

References 31 publications

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“…Under our experimental conditions, although a remarkable antiproliferative effect could be achieved when combining ATO with sanguinarine, the optimal effect was obtained with the concomitant treatment including TRAIL. Our findings are Rational TRAIL-Based Combinations in Lung Cancer Cells consistent with the reports showing that sanguinarine sensitizes human tumor cells to TRAIL-mediated apoptosis (Choi et al, 2009) and induces apoptosis of human tumor cells through the activation of the extrinsic pathway (Park et al, 2010).…”

Section: Tablesupporting

confidence: 92%

“…In fact, sanguinarine induces apoptosis in a variety of cancer cells after cell cycle arrest (Adhami et al, 2004), caspase activation (Kim et al, 2008), depletion of cellular GSH (Debiton et al, 2003), modulation of Bcl-2 family members (Ahsan et al, 2007;Lee et al, 2012;Xu, et al, 2012), and upregulation of death receptor 5 [DR5; tumor necrosis factor-related apoptosis-inducing ligand R2 (TRAIL-R2)] (Hussain et al, 2007). Of note, it has been observed that sanguinarine sensitizes human gastric adenocarcinoma cells to TRAIL-mediated apoptosis (Choi et al, 2009) and that it induces apoptosis of human osteosarcoma cells through the extrinsic pathway (Park et al, 2010). Because of its preferential ability to induce apoptosis in cancer cells over normal cells (Ichikawa et al, 2001), TRAIL can be regarded as a promising targeted drug (Takeda et al, 2007) which induces apoptosis in a variety of cancer cells by interacting with its death receptors DR4 (TRAIL-R1) and DR5 (TRAIL-R2) on the target cell surface (Johnstone et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

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Improved Apoptotic Cell Death in Drug-Resistant Non–Small-Cell Lung Cancer Cells by Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Based Treatment

Gatti

Cossa

Tinelli

et al. 2013

J Pharmacol Exp Ther

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Since response to platinum-based therapy in non-small-cell lung cancer (NSCLC) is poor, the present study was designed to rationally identify novel drug combinations in cell models including the A549 cell line and the cisplatin-resistant subline A549/Pt, characterized by reduced sensitivity to cisplatin-induced apoptosis and by upregulation of efflux transporters of the ATP binding cassette (ABC) superfamily. Given the molecular features of these cells, we focused on compounds triggering apoptosis through different mechanisms, such as the mitochondria-targeting drug arsenic trioxide and the phenanthridine analog sanguinarine, which induce apoptosis through the extrinsic pathway. Sanguinarine, not recognized by ABC transporters, could overcome cisplatin resistance and, when used in combination with arsenic trioxide, was synergistic in A549 and A549/Pt cells. The arsenic trioxide/sanguinarine cotreatment upregulated genes implicated in apoptosis activation through the extrinsic pathway. Drug combination experiments indicated that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) treatment improved arsenic trioxide/sanguinarine efficacy, a feature associated with a striking apoptosis induction, particularly in the cisplatin-resistant variant. Thus, a synergistic interaction between sanguinarine and arsenic trioxide could be obtained independent of relative cell sensitivity to arsenic trioxide, and an enhanced apoptosis induction could be achieved in combination with TRAIL through modulation of the extrinsic apoptotic pathway. Antitumor activity studies supported the interest of drug combinations including TRAIL in NSCLC, indicating that drug-resistant NSCLC cells can efficiently be killed by the combination of proapoptotic agents. Our results suggest that the molecular changes occurring in treated cells may be exploited to rationally hit surviving cells.

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Section: Tablesupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Improved Apoptotic Cell Death in Drug-Resistant Non–Small-Cell Lung Cancer Cells by Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Based Treatment

Gatti

Cossa

Tinelli

et al. 2013

J Pharmacol Exp Ther

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“…In detail, it has been reported that micromolar concentrations of sanguinarine are capable of inhibiting tumor cell growth, and this inhibitory effect is associated with cell cycle arrest and induction of apoptosis [19][20][21][22] . The anti-proliferative and/ or pro-apoptotic activities of sanguinarine have been demonstrated in in vitro studies on several cancer cell types including epidermal [23] , keratinocyte [24,25] , prostate [26][27][28] , cervical [29] , breast [20,[30][31][32][33] , leukaemia [34,35] , lymphoma [36] , melanoma [37][38][39] , colon [40,41] , colorectal [21] , gastric [42] , pancreatic [19] , lung [22] , neuroendocrine [43] , osteosarcoma [44] , and human neuroblastoma cells [45] . By contrast, there are few studies on the in vivo effectiveness of sanguinarine administration per os [46,47] in animal tumor models [33,48] .…”

Section: Sanguinarine Induces Apoptosis In Tumor Cellsmentioning

confidence: 99%

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Gaziano

Moroni

Buè

et al. 2016

WJGO

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Historically, natural products have represented a significant source of anticancer agents, with plant-derived drugs becoming increasingly explored. In particular, sanguinarine is a benzophenanthridine alkaloid obtained from the root of Sanguinaria canadensis , and from other poppy Fumaria species, with recognized anti-microbial, anti-oxidant and anti-inflammatory properties. Recently, increasing evidence that sanguinarine exibits anticancer potential through its capability of inducing apoptosis and/or antiproliferative effects on tumor cells, has been proved. Moreover, its antitumor seems to be due not only to its pro-apoptotic and inhibitory effects on tumor growth, but also to its antiangiogenic and anti-invasive properties. Although the precise mechanisms underlying the antitumor activity of this compound remain not fully understood, in this review we will focus on the most recent findings about the cellular and molecular pathways affected by sanguinarine, together with the rationale of its potential application in clinic. The complex of data currently available suggest the potential application of sanguinarine as an adjuvant in the therapy of cancer, but further pre-clinical studies are needed before such an antitumor strategy can be effectively translated in the clinical practice.

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“…The antiproliferative and/or pro-apoptotic activities of sanguinarine have been demonstrated in cells derived from several human cancers including epidermal (Ahmad et al, 2000), keratinocytes (Adhami et al, 2003;Reagan-Shaw et al, 2006), prostate (Malikova et al, 2006b;Adhami et al, 2004;Huh et al, 2006), cervical (Ding et al, 2002), breast Debiton et al, 2003;Holy et al, 2006), leukemia (Han et al, 2008;Weerasinghe et al, 2001c;Weerasinghe et al, 2001b;Weerasinghe et al, 2001a), lymphoma (Hussain et al, 2007), melanoma (Burgeiro et al, 2013;Hammerova et al, 2011;Serafim et al, 2008), colon (Lee et al, 2012;Matkar et al, 2008), colorectal (Han et al, 2013a;Lee et al, 2012;Pica et al, 2012), gastric (Choi et al, 2009), pancreatic (Ahsan et al, 2007), lung (Jang et al, 2009), neuroendocrine (Larsson et al, 2010), osteosarcoma (Park et al, 2010), and in rat glioblastoma cells (Han et al, 2007), bladde (Han et al, 2013b). However, the impact of sanguinarine on neuroblastoma cells has not been shown.…”

Section: Discussionmentioning

confidence: 99%

Promoting Effects of Sanguinarine on Apoptotic Gene Expression in Human Neuroblastoma Cells

Çeçen¹,

Altun²,

Erçetin³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Neuroblastoma is the most common extracranial solid tumor in children. Approximately half of the affected patients are diagnosed with high-risk poor prognosis disease, and novel therapies are needed. Sanguinarine is a benzophenanthridine alkaloid which has anti-microbial, anti-oxidant and anti-inflammatory properties. The aim of this study is whether sanguinarine has in vitro apoptotic effects and which apoptotic genes might be affected in the human neuroblastoma cell lines SH-SY5Y (N-myc negative), Kelly (N-myc positive, ALK positive), and SK-N-BE(2). Cell viability was analysed with WST-1 and apoptotic cell death rates were determined using TUNEL. After RNA isolation and cDNA conversion, expression of 84 custom array genes of apoptosis was determined. Sanguinarine caused cell death in a dose dependent manner in all neuroblastoma cell lines except SK-N-BE(2) with rates of 18% in SH-SY5Y and 21% in Kelly human neuroblastoma cells. Cisplatin caused similar apoptotic cell death rates of 16% in SH-SY5Y and 23% in Kelly cells and sanguinarine-cisplatin combinations caused the same rates (18% and 20%). Sanguinarine treatment did not affect apoptototic gene expression but decreased levels of anti-apoptotic genes NOL3 and BCL2L2 in SH-SY5Y cells. Caspase and TNF related gene expression was affected by the sanguinarine-cisplatin combination in SH-SY5Y cells. The expression of regulation of apoptotic genes were increased with sanguinarine treatment in Kelly cells. From these results, we conclude that sanguinarine is a candidate agent against neuroblastoma.

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Sanguinarine induces apoptosis of human osteosarcoma cells through the extrinsic and intrinsic pathways

Cited by 50 publications

References 31 publications

Improved Apoptotic Cell Death in Drug-Resistant Non–Small-Cell Lung Cancer Cells by Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Based Treatment

Improved Apoptotic Cell Death in Drug-Resistant Non–Small-Cell Lung Cancer Cells by Tumor Necrosis Factor–Related Apoptosis-Inducing Ligand–Based Treatment

Antitumor effects of the benzophenanthridine alkaloid sanguinarine: Evidence and perspectives

Promoting Effects of Sanguinarine on Apoptotic Gene Expression in Human Neuroblastoma Cells

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