Sanguinarine causes DNA damage and p53-independent cell death in human colon cancer cell lines

Matkar, Smita; Wrischnik, Lisa A.; Hellmann-Blumberg, Utha

doi:10.1016/j.cbi.2007.12.006

Cited by 66 publications

(52 citation statements)

References 38 publications

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“…Apoptosis caused by sanguinarine has been shown through different ways, such as mitochondrial damage, nuclear factor kappa-light-chain enhancer of activated B cells activation, and cell cycle arrest [2] . Sanguinarine is shown to inhibit microtubule polymerization and can intercalate double-stranded DNA [3,4] . The caspase activation, depletion of cellular glutathione, downregulation of extracellular signal-regulated kinases, modulation of B-cell lymphoma 2 family, and upregulation of DR-5 are the mechanisms of antitumoral action of sanguinarine [4][5][6][7] .…”

Section: Introductionmentioning

confidence: 99%

“…Sanguinarine is shown to inhibit microtubule polymerization and can intercalate double-stranded DNA [3,4] . The caspase activation, depletion of cellular glutathione, downregulation of extracellular signal-regulated kinases, modulation of B-cell lymphoma 2 family, and upregulation of DR-5 are the mechanisms of antitumoral action of sanguinarine [4][5][6][7] . It is shown that the cytotoxic activity of benzophenanthridine is propotional to the DNA-binding feature and induction of DNA fragmentation.…”

Section: Introductionmentioning

confidence: 99%

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Apoptotic Effects of Sanguinarine on the Organ of Corti 1 Cells: Comparison with Cisplatin

Çeçen¹,

Erçetin²,

Kırkım³

et al. 2015

Int Adv Otol

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OBJECTIVE:Sanguinarine is an alkaloid obtained from the root of Sanguinaria canadensis and other plants from the Papaveraceae family and is well known to possess a broad range of biological functions, such as antimicrobial, antifungal, anti-inflammatory, and antineoplastic activities. We aimed to specify the in vitro effect of sanguinarine on the House Ear Institute-Organ of Corti 1 (HEI-OC1) cells and to compare this effect with the ototoxic effect of cisplatin (CDDP). MATERIALS and METHODS:We performed cell proliferation assay for determining the in vitro effect of sanguinarine alone and compared it with the effect of cisplatin. Flow cytometry annexin-V apoptosis detection was performed. RESULTS:We found that sanguinarine and CDDP inhibited the cell growth in a dose-dependant manner in HEI-OC1 cells after 24 h of incubation. In sanguinarine-treated group, apoptosis was 6.6%, necrosis was 26.7%, and the cell viability was 66.7%. Further, in CDDP-treated group, apoptosis was 5.6%, necrosis was 45.4%, and the cell viability was 48.7%. According to the annexin-V apoptosis detection results, we found that sanguinarine caused 3.9% apoptosis and 1.3% necrosis, while CDDP caused 2.9% apoptosis and 20% necrosis on HEI-OC1 cells. CONCLUSION:Our findings suggested that lower doses of sanguinarine are promising antineoplastic agents, which did not indicate any toxic effect on HEI-OC1 cells. Application of these data to clinical practice requires further support by in vivo studies.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Apoptotic Effects of Sanguinarine on the Organ of Corti 1 Cells: Comparison with Cisplatin

Çeçen¹,

Erçetin²,

Kırkım³

et al. 2015

Int Adv Otol

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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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“…그러나 이러한 현상 은 암세포 특이적으로 나타나며, TRAIL이 apoptosis 유도를 통한 항암효능 증대에 대한 phase 2 clinical trial에 적용되고 있지만, 많은 암세포들이 이미 TRAIL에 대한 저항성을 획득 하고 있다는 점에서 TRAIL의 감수성을 탁월하게 높일 수 있 는 물질의 발굴이 시급한 실정이다 [4,31]. [16,20,23,24,26]. 최근 본 연구실의 결과에 의하면, sanguinarine은 교아종(glioblastoma) 세포에서 mitogen activated 생성 의존적 미토콘드리아 활성화를 통하여 일어났음을 알 수 있었고 [7], 인체 유방암세포의 전이 억제는 치밀 결합(tight junction)의 활성 증가와 matrix metalloproteinase 활성 증가 와 연관성이 있었다 [6].…”

Section: 서 론unclassified

“…3). Sanguinarine 및 TRAIL 복합처리에 의한 apoptosis 유 발에서 ROS의 역할 다음은 유방암세포를 이용한 선행 연구에서 sanguinarine 에 의한 apoptosis 유발에 ROS의 생성이 필수적으로 동반된 다는 보고 [7,13,14,16,21,24]를 바탕으로, sanguinarine과 TRAIL 복합처리에 의한 AGS 세포의 apoptosis 유발에서도 ROS 생성이 관련되어 있는지의 여부를 조사하였다. [3, 7, 11, 12-14, 16, 20, 21, 24] …”

Section: Sanguinarine과 Trail의 복합처리에 의한 Dr5 발현의 증가unclassified

Sanguinarine Increases Sensitivity of Human Gastric Adenocarcinoma Cells to TRAIL-mediated Apoptosis by Inducing DR5 Expression and ROS Generation

Lee¹,

Im²,

Choi³

et al. 2014

Journal of Life Science

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Sanguinarine, a benzophenanthridine alkaloid originally derived from the root of Sanguinaria canadensis, has been shown to possess antimicrobial, antioxidant, and anti-cancer properties. Although tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is known to induce apoptosis in cancer cells, but not most normal cells and has shown efficacy in a phase 2 clinical trial, development of resistance to TRAIL by tumor cells is a major roadblock. Our previous study indicated that treatment with TRAIL in combination with subtoxic concentrations of sanguinarine sensitized TRAIL-mediated apoptosis in TRAIL-resistant human gastric carcinoma AGS cells; however, the detailed mechanisms are not fully understood. In this study, we show that sanguinarine sensitizes AGS cells to TRAILmediated apoptosis as detected by MTT assay, agarose gel electrophoresis, chromatin condensation and flow cytometry analysis. Combined treatment with sanguinarine and TRAIL effectively induced expression of death receptor (DR) 5 but did not affect expression of DR4 and mitogen activated protein kinases signaling molecules. Moreover, the combined treatment with sanguinarine and TRAIL increased the generation of reactive oxygen species (ROS); however, N-acetylcysteine, ROS scavenger, significantly recovered growth inhibition induced by the combined treatment. Taken together, our results indicate that sanguinarine can potentiate TRAIL-mediated apoptosis through up-regulation of DR5 expression and ROS generation. 다[16, 20, 23, 24, 26]. 최근 본 연구실의 결과에 의하면, sanguinarine은 교아종(glioblastoma) 세포에서 mitogen activated

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Sanguinarine causes DNA damage and p53-independent cell death in human colon cancer cell lines

Cited by 66 publications

References 38 publications

Apoptotic Effects of Sanguinarine on the Organ of Corti 1 Cells: Comparison with Cisplatin

Apoptotic Effects of Sanguinarine on the Organ of Corti 1 Cells: Comparison with Cisplatin

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

Sanguinarine Increases Sensitivity of Human Gastric Adenocarcinoma Cells to TRAIL-mediated Apoptosis by Inducing DR5 Expression and ROS Generation

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