ArticleCell proliferation2010
Combination of photodynamic therapy with aspirin in human-derived lung adenocarcinoma cells affects proteasome activity and induces apoptosis.
Article in Cell proliferation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Photodynamic therapy with 5-aminolaevulinic acid and DNA damage: unravelling roles of p53 and ABCG2.Cell proliferation · 2016Article
- Mitochondrial Malfunctioning, Proteasome Arrest and Apoptosis in Cancer Cells by Focused Intracellular Generation of Oxygen Radicals.International journal of molecular sciences · 2015Article
- 5-aminolaevulinic acid/photo-dynamic therapy and gefitinib in non-small cell lung cancer cell lines: a potential strategy to improve gefitinib therapeutic efficacy.Cell proliferation · 2013Article
- Comparisons of 5-aminolevulinic acid photodynamic therapy and after-loading radiotherapy in vivo in cervical cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2013Article
- Enhancing photodynamyc therapy efficacy by combination therapy: dated, current and oncoming strategies.Cancers · 2011Article
- Targets and mechanisms of photodynamic therapy in lung cancer cells: a brief overview.Cancers · 2011Article
- New hydrophilic/lipophilic tetra-α-(4-carboxyphenoxy) phthalocyanine zinc-mediated photodynamic therapy inhibits the proliferation of human hepatocellular carcinoma Bel-7402 cells by triggering apoptosis and arresting cell cycle.Molecules (Basel, Switzerland) · 2011Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesPhotodynamic treatment (PDT) of human lung carcinoma cells A549 (p53(+/+)) and H1299 (p53(-/-)) induces fast but transient stalling of proteasome activity. We have explored the possibility of prolonging this effect by combining PDT with drugs capable of sustaining the stall, and promote apoptosis of surviving cells. We show that aspirin can be used to accomplish this. MATERIALS AND
methodsCells were irradiated at doses ranging from 0.54 to 1.10 J cm(-2), and subsequently were incubated with aspirin at either high (10 and 5 mm) or low concentration (2.5 and 1.5 mm). Photofrin concentration and incubation time were constant (2.5 μg/ml and 16 h). Under these conditions, we analysed cell viability, colony-forming efficiency, cycle profile, expression patterns of specific proteins and ubiquitination state, after individual or combined administration.
resultsTreatment with either PDT or aspirin, rapidly induced proteasome malfunction and accumulation of cells in G(2)M, but did not induce apoptosis. However, when aspirin was added to cells (even at low concentrations) after PDT, the proteasome block was sustained. Moreover, significant cytotoxic effects, including apoptosis, were observed along with cytostatic effects (G(2)M accumulation/decreased colony formation).
conclusionsCombination of PDT and low-toxicity drugs (such as aspirin) resulted in protracted inhibition of proteasome activity and induced apoptosis even in apoptosis-resistant cancer cells.
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