ArticlePloS one2018
Dexamethasone modified by gamma-irradiation as a novel anticancer drug in human non-small cell lung cancer.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 7 citations in OpenAlex.
- Ionizing radiation‑induced modification of nialamide as an anti‑inflammatory agent against lipopolysaccharide‑induced RAW 264.7 and DH82 cells.Experimental and therapeutic medicine · 2024Article
- Dexamethasone and OLT1177 Cooperate in the Reduction of Melanoma Growth by Inhibiting STAT3 Functions.Cells · 2023Article
- Transformation of nomifensine using ionizing radiation and exploration of its anticancer effects in MCF-7 cells.Experimental and therapeutic medicine · 2022Article
- γ‑irradiated prednisolone promotes apoptosis of liver cancer cells via activation of intrinsic apoptosis signaling pathway.Molecular medicine reports · 2021Article
- A novel radiolytic rotenone derivative, rotenoisin A, displays potent anticarcinogenic activity in breast cancer cells.Journal of radiation research · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dexamethasone (Dex) is widely used in the management of leukemia and lymphoma. While Dex is commonly used for hematological malignancies, the effects of Dex in solid cancer cells remain controversial. To develop a more effective anticancer drug for solid cancers, Dex was modified by ionizing radiation and the anticancer activity of ionizing-radiation-irradiated Dex (Dex-IR) was investigated in human lung cancer cells. Using the MTT assay, the proliferation of non-small cell lung cancer cells was significantly inhibited after treatment with Dex-IR compared with Dex. Furthermore, Dex-IR induced apoptotic cell death and cell cycle arrest of H1650 human lung cancer cells. The invasiveness of H1650 cells was significantly reduced and the matrix metalloproteinase activity was strongly suppressed. These results indicate that Dex-IR acts as a tumor suppressor by both inducing apoptosis and arresting the cell cycle. Although the structure of Dex-IR remains to be determined, our results suggest it may be useful as a novel anticancer agent for the treatment of solid cancers.
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Registered trials
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