ArticleInternational journal of physiology, pathophysiology and pharmacology2012
Selective toxicity of rose bengal to ovarian cancer cells in vitro.
Article in International journal of physiology, pathophysiology and pharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
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- A study of Rose Bengal against a 2-keto-3-deoxy-d-Journal of enzyme inhibition and medicinal chemistry · 2020Article
- Development of an Oil-in-Water Self-Emulsifying Microemulsion for Cutaneous Delivery of Rose Bengal: Investigation of Anti-Melanoma Properties.Pharmaceutics · 2020Article
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- Colon cancer cell treatment with rose bengal generates a protective immune response via immunogenic cell death.Cell death & disease · 2017Article
- Intralesional rose bengal in melanoma elicits tumor immunity via activation of dendritic cells by the release of high mobility group box 1.Oncotarget · 2016Article
- The Potential of Intralesional Rose Bengal to Stimulate T-Cell Mediated Anti-Tumor Responses.Journal of clinical & cellular immunology · 2015Article
- Fabrication of three-dimensional multi-protein microstructures for cell migration and adhesion enhancement.Biomedical optics express · 2015Article
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rose bengal (RB) has been utilized as a photodynamic agent for the targeted killing of cancer cells. Recent data suggest that intralesional RB alone may be effective in chemoablating locoregional and metastatic melanomas. The ability of RB to induce direct and bystander melanoma cell death led to the speculation that it may be similarly effective in the treatment of other neoplasms. The objective of this study was to determine whether RB can limit the growth, or kill, ovarian cancer cells in vitro. Ovarian carcinoma cells with or without a germline BRCA1 mutation were cultured with up to 800 μM RB for one hour or four days, after which their ability to proliferate was assessed using the MTT assay. Control cells included an embryonic kidney cell line transformed with adenovirus, and normal human fibroblasts. Ovarian cancer cells exhibited significant dose-dependent suppression of growth in response to RB; this suppression was similar to that seen with carboplatin. RB treated ovarian cancer cells appeared rounded, shrunken, and damaged. RB also inhibited the growth of kidney tumor cells but was much less effective in slowing the growth of normal human fibroblasts suggesting that RB-mediated growth suppression might be tumor cell specific. Ovarian cancer cells treated with RB displayed a significant increase in apoptosis that peaked at approximately four times the levels seen in untreated control cells. Furthermore, RB exposure resulted in the intracellular generation of reactive oxygen species (ROS) at levels that were significantly greater than in untreated cells and similar to levels seen in cells treated short term with H(2)O(2). These data suggest that RB may not only suppress ovarian cancer cell growth but also induce their apoptotic cell death, justifying the further investigation of the effects of RB in an animal model of ovarian cancer.
Indexed as
Identifiers
22837809PMC3403562W1586481898What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.