Sodium nitroprusside (SNP) sensitizes human gastric cancer cells to TRAIL-induced apoptosis

Yang, Liu-Qin; Lan, Chun‐Hui; Yu, Fang; Zhang, Yafei; Wang, Jun; Guo, Jianbin; Wan, Suigui; Yang, Shi‐Ming; Wang, Rong-quan; Fang, Dian‐Chun

doi:10.1016/j.intimp.2013.06.021

Cited by 25 publications

(28 citation statements)

References 34 publications

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“…29 It was recently reported that SNP sensitized AGS, SGC7901, MKN45, and MKN28 gastric cancer cell lines to tumor necrosis factor (TNF) related apoptosisinducing ligand (TRAIL) induced apoptosis. 43 However, the in vivo effects of SNP were not investigated due to the spontaneous and nonselective NO release. NO-coordinated ruthenium complexes constitute another class of NO donors with the general structure trans-[Ru II (NO + )(L 1 ) x (L 2 )] n+ , which can be thermally or photochemically activated to release NO.…”

Section: Journal Of Medicinal Chemistrymentioning

confidence: 99%

Nitric Oxide Donor-Based Cancer Therapy: Advances and Prospects

2017

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The increasing understanding of the role of nitric oxide (NO) in cancer biology has generated significant progress in the use of NO donor-based therapy to fight cancer. These advances strongly suggest the potential adoption of NO donor-based therapy in clinical practice, and this has been supported by several clinical studies in the past decade. In this review, we first highlight several types of important NO donors, including recently developed NO donors bearing a dinitroazetidine skeleton, represented by RRx-001, with potential utility in cancer therapy. Special emphasis is then given to the combination of NO donor(s) with other therapies to achieve synergy and to the hybridization of NO donor(s) with an anticancer drug/agent/fragment to enhance the activity or specificity or to reduce toxicity. In addition, we briefly describe inducible NO synthase gene therapy and nanotechnology, which have recently entered the field of NO donor therapy.

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Section: Journal Of Medicinal Chemistrymentioning

confidence: 99%

Nitric Oxide Donor-Based Cancer Therapy: Advances and Prospects

2017

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“…TRAIL induces cancer cell apoptosis via an “extrinsic”, death-receptor-mediated pathway. Numerous studies have shown that compounds stimulating the “intrinsic”, mitochondria-dependent apoptotic pathway potentiate tumors to apoptotic induction by TRAIL [18,19,20,21]. Thus, mitochondrion is proposed as a direct target for the development of effective TRAIL sensitizers [19].…”

Section: Discussionmentioning

confidence: 99%

CYC1 Silencing Sensitizes Osteosarcoma Cells to TRAIL-Induced Apoptosis

Liang

et al. 2014

Cell Physiol Biochem

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Aims: Osteosarcoma (OS) is an aggressive bone malignancy with poor prognosis. Many OS cells are resistant to apoptotic induction by tumor necrosis factor-related apoptosis inducing ligand (TRAIL). In our previous study, we found that the serum level of cytochrome c1 (CYC1) is significantly higher in OS patients than in healthy subjects. Our aim was to investigate the effects of CYC1 silencing on TRAIL-induced apoptosis in human OS in vitro and in vivo along with the underlying mechanisms. Methods: First, we determined the expression of CYC1 in human OS tumors and cell lines versus normal adjacent tissues and cell line. We then studied the effects of CYC1 silencing alone or in combination with TRAIL on OS cell growth and apoptosis in vitro and OS tumorigenesis in vivo. Results: We found that CYC1 is overexpressed in human OS tissues and cell lines. CYC1 silencing by shRNA transfection inhibits proliferation, slightly induces apoptosis in human OS cells in vitro, and suppresses human OS tumor growth in a mouse xenograft model in vivo. Additionally, CYC1 silencing sensitizes OS to TRAIL-induced apoptosis in vitro and in vivo. Our results also showed that CYC1 silencing significantly reduces complex III activity and potentiates TRAIL-induced cytochrome c release and caspase-9 activation in OS cells, suggesting that CYC1 silencing acts via the mitochondria-dependent apoptotic pathway. Conclusion: Taken together, our results provide evidence that CYC1 plays an important role in OS tumorigenesis, and modulation of CYC1 may be an effective strategy to potentiate OS to apoptotic induction by TRAIL.

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“…It has been found that SNP enhanced the cytotoxicity mediated by tumor necrosis‐related apoptosis‐inducing ligand (TRAIL) in gastric cancer cells AGS, MKN45, MKN28, and SGC‐7901, which further promoted mitochondrial‐mediated apoptotic signal transduction pathways, including the activation of caspase‐8 and caspase‐9. [ 96 ] Liaw's team synthesized dinitrosyl iron complexes [Fe 2 (µ‐SCH 2 CH 2 OH) 2 (NO) 4 ] (DNIC‐1) that continuously released NO (16.8 ± 1.8 h at 37 °C). DNIC‐1 could more effectively activate angiogenesis and promote wound healing than Spermine NONOate and MAHMA NONOate in diabetic mice.…”

Section: Application Of No In Immunotherapymentioning

confidence: 99%

Progress and Prospects of Regulatory Functions Mediated by Nitric Oxide on Immunity and Immunotherapy

Shi

Jiao

et al. 2021

Advanced Therapeutics

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Nitric oxide (NO), as a crucial signaling biomolecule, is closely involved in the cardiovascular, immune, and central nervous system. NO not only participates in the proliferation, differentiation, and activation of immune cells but also regulates the secretion and function of immune-related cytokines. Meanwhile, NO plays an important role in regulating diversified pathological processes, such as cancer, autoimmune disease, pathogenic infection, and so on. Therefore, the intensive immunological study of NO has been expected to provide valuable approaches to the clinical prevention and treatment of these related diseases. Since NO has a wide range of chemical activities and biological functions, the pleiotropic effects of NO are affected by its production, concentration and duration, target cell types and subtypes, species, and pathogenesis of the immune-related diseases. It is thus necessary to create and develop certain platforms of drugs and related preparations that can precisely regulate NO for immunotherapy. This review summarizes the regulatory functions exerted by NO in immune response, and the pathological mechanisms of tumor, autoimmune disease, and pathogenic infection in which NO is involved. The application and trend of therapeutic strategies based on the direct regulation of NO in immunotherapy are further discussed.

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Sodium nitroprusside (SNP) sensitizes human gastric cancer cells to TRAIL-induced apoptosis

Cited by 25 publications

References 34 publications

Nitric Oxide Donor-Based Cancer Therapy: Advances and Prospects

Nitric Oxide Donor-Based Cancer Therapy: Advances and Prospects

CYC1 Silencing Sensitizes Osteosarcoma Cells to TRAIL-Induced Apoptosis

Progress and Prospects of Regulatory Functions Mediated by Nitric Oxide on Immunity and Immunotherapy

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