ArticleArchives of medical science : AMS2015
Influence of PJ34 on the genotoxicity induced by melphalan in human multiple myeloma cells.
Article in Archives of medical science : AMS, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Targeting the DNA damage response in hematological malignancies.Frontiers in oncology · 2024Review
- Novel Macrolactams from a Deep-Sea-DerivedMarine drugs · 2020Article
- The Modified Phenanthridine PJ34 Unveils an Exclusive Cell-Death Mechanism in Human Cancer Cells.Cancers · 2020Review
- New Ansamycins from the Deep-Sea-Derived BacteriumMarine drugs · 2018Article
- Impact of lenalidomide exposure on blood cell collection for autotransplants in persons with POEMS syndrome.Archives of medical science : AMS · 2018Article
- Advances in the understanding of Fanconi Anemia Complementation Group D2 Protein (FANCD2) in human cancer.Cancer cell & microenvironmentArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe aim of this study was to evaluate the potential biological activity of N-(6-oxo-5,6-dihydrophenanthridin-2-yl)-(N,N-dimethylamino)acetamide hydrochloride (PJ34) on the genotoxicity induced by melphalan in human multiple myeloma cells. MATERIAL AND
methodsThe inhibitory effects of the drugs on the growth of RPMI8226 cells were determined by Cell Counting Kit-8 (CCK-8) assay. The expression of Fanconi anemia/breast cancer (FA/BRCA) pathway related genes was determined by western blot analysis. Cell cycle phase and apoptosis were analyzed by flow cytometry. Coadministration of PJ34 and melphalan had additional effects on cell cycle distribution and enhanced apoptosis of RPMI8226 cells. PJ34 plus melphalan inhibited cell-cycle progression, as evidenced by the increased proportion of cells in the G2/M phase with the decreasing proportion of cells in the G0/1 and S phases.
resultsHowever, no significant synergistic effect of PJ34 and melphalan on cell proliferation was observed. These effects were accompanied by inhibition of the FA/BRCA pathway by downregulation of Fanconi D2 (FANCD2) protein expression. The results showed that treatment with 60 µmol/l of PJ34 previously to melphalan administration increased cell apoptosis. Pretreatment also caused cell cycle arrest.
conclusionsThis study suggests that enhancement of melphalan efficacy may be best achieved by the poly(ADP-ribose) polymerase-1 (PARP-1) inhibitor PJ34. The effects of PJ34 are associated with inhibition of the FA/BRCA pathway, increased apoptosis percentage, and G2/M cell cycle arrest. Administration of PJ34 has been shown to protect DNA from damage induced by melphalan. This corroborates the biological activities of PJ34 and points to the need for further studies.
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