Synthesis and evolution of S-Porphin sodium as a potential antitumor agent for photodynamic therapy against breast cancer

2019 ◽  
Vol 6 (3) ◽  
pp. 362-372 ◽  
Author(s):  
Xiao Wang ◽  
Li Li ◽  
Kun Zhang ◽  
Zhen Han ◽  
Zhijian Ding ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Tumor Cell ◽  
Antitumor Agent ◽  
The Novel ◽  
Tumor Cell Death ◽  
Long Wavelength ◽  
Potential Antitumor

The novel sensitizer S-Porphin sodium can generate ROS by radiation with a long wavelength to cause tumor cell death.

Photodynamic Therapy with Liposomal Zinc Phthalocyanine and Tirapazamine Increases Tumor Cell Death via DNA Damage

2017 ◽  
Vol 13 (2) ◽  
pp. 204-220 ◽  
Author(s):  
Mans Broekgaarden ◽  
Ruud Weijer ◽  
AlbertC. van Wijk ◽  
RuudC. Cox ◽  
MaartenR. Egmond ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Photodynamic Therapy ◽  
Tumor Cell ◽  
Zinc Phthalocyanine ◽  
Tumor Cell Death

scholarly journals Enhancement of Tumor Cell Death by Combining gef Gene Mediated Therapy and New 1,4-Benzoxazepin-2,6-Dichloropurine Derivatives in Breast Cancer Cells

2018 ◽  
Vol 9 ◽  
Author(s):  
Alberto Ramírez ◽  
Ana Conejo-García ◽  
Carmen Griñán-Lisón ◽  
Luisa C. López-Cara ◽  
Gema Jiménez ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Tumor Cell ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Tumor Cell Death

Personalization of breast cancer chemotherapy using noninvasive imaging methods to detect tumor cell death responses

2014 ◽  
Vol 3 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lakshmanan Sannachi ◽  
Hadi Tadayyon ◽  
Ali Sadeghi-Naini ◽  
Michael C Kolios ◽  
Gregory Czarnota
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Tumor Cell ◽  
Cancer Chemotherapy ◽  
Noninvasive Imaging ◽  
Tumor Cell Death ◽  
Imaging Methods ◽  
Breast Cancer Chemotherapy

scholarly journals Computational pharmacogenomics screen identifies synergistic statin-compound combinations as anti-breast cancer therapies

2020 ◽  
Author(s):  
Jenna van Leeuwen ◽  
Wail Ba-Alawi ◽  
Emily Branchard ◽  
Joseph Longo ◽  
Jennifer Silvester ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Death ◽  
Tumor Cell ◽  
Mevalonate Pathway ◽  
Parent Compound ◽  
Antiplatelet Agent ◽  
Breast Cancer Cell Lines ◽  
Tumor Cell Death ◽  
Mesenchymal Transition ◽  
Pathway Gene

AbstractStatins are a family of FDA-approved cholesterol-lowering drugs that inhibit the rate-limiting enzyme of the metabolic mevalonate pathway, which have been shown to have anti-cancer activity. As therapeutic efficacy is increased when drugs are used in combination, we sought to identify agents, like dipyridamole, that potentiate statin-induced tumor cell death. As an antiplatelet agent dipyridamole will not be suitable for all cancer patients. Thus, we developed an integrative pharmacogenomics pipeline to identify agents that were similar to dipyridamole at the level of drug structure, in vitro sensitivity and molecular perturbation. To enrich for compounds expected to target the mevalonate pathway, we took a pathway-centric approach towards computational selection, which we called mevalonate drug network fusion (MVA-DNF). We validated two of the top ranked compounds, nelfinavir and honokiol and demonstrated that, like dipyridamole, they synergize with fluvastatin to potentiate tumor cell death by blocking the restorative feedback loop. This is achieved by inhibiting activation of the key transcription factor that induces mevalonate pathway gene transcription, sterol regulatory element-binding protein 2 (SREBP2). Mechanistically, the synergistic response of fluvastatin+nelfinavir and fluvastatin+honokiol was associated with similar transcriptomic and proteomic pathways, indicating a similar mechanism of action between nelfinavir and honokiol when combined with fluvastatin. Further analysis identified the canonical epithelial-mesenchymal transition (EMT) gene, E-cadherin as a biomarker of these synergistic responses across a large panel of breast cancer cell lines. Thus, our computational pharmacogenomic approach can identify novel compounds that phenocopy a compound of interest in a pathway-specific manner.Significance StatementWe provide a rapid and cost-effective strategy to expand a class of drugs with a similar phenotype. Our parent compound, dipyridamole, potentiated statin-induced tumor cell death by blocking the statin-triggered restorative feedback response that dampens statins pro-apoptotic activity. To identify compounds with this activity we performed a pharmacogenomic analysis to distinguish agents similar to dipyridamole in terms of structure, cell sensitivity and molecular perturbations. As dipyridamole has many reported activities, we focused our molecular perturbation analysis on the pathway inhibited by statins, the metabolic mevalonate pathway. Our strategy was successful as we validated nelfinavir and honokiol as dipyridamole-like drugs at both the phenotypic and molecular levels. Our pathway-specific pharmacogenomics approach will have broad applicability.

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