ArticleOncology letters2014
Inhibition of mammalian target of rapamycin by rapamycin increases the radiosensitivity of esophageal carcinoma Eca109 cells.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Potential Molecular Targets in the Setting of Chemoradiation for Esophageal Malignancies.Journal of the National Cancer Institute · 2021Review
- lncRNA KLF3-AS1 Suppresses Cell Migration and Invasion in ESCC by Impairing miR-185-5p-Targeted KLF3 Inhibition.Molecular therapy. Nucleic acids · 2020Article
- mTOR-Mediated Antioxidant Activation in Solid Tumor Radioresistance.Journal of oncology · 2019Review
- Enhancement of mTOR signaling contributes to acquired X-ray and C-ion resistance in mouse squamous carcinoma cell line.Cancer science · 2017Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of the present study was to investigate whether radiation induces the mammalian target of rapamycin (Rap) (mTOR) signaling pathway in esophageal carcinoma Eca109 cells, and whether mTOR inhibition by rapamycin increases Eca109 cell radiosensitivity. Changes in the levels of mTOR signaling pathway and DNA damage-repair proteins in Eca109 cells prior to and following radiation were determined. The Eca109 cells were treated with Rap (0, 100, 200 and 400 nmol/l) in combination with radiation (0, 2, 4 and 6 Gy). The cell proliferation inhibition rate was determined by MTT assay. The optimum Rap concentration and radiation dose, which appropriately inhibited cell proliferation, were then selected for further study. An appropriate combination of Rap and radiation for the Eca109 cells was also selected and changes in the mTOR signaling pathway, apoptosis and DNA damage-repair proteins, as well as in cell clone formation, survival curves, the apoptosis rate and radiation-induced DNA damage were determined. The expression of the mTOR signaling pathway and DNA damage-repair proteins were found to increase following the irradiation of the Eca109 cells. In addition, Rap was found to inhibit the mTOR signaling pathway and the expression of the DNA damage-repair proteins. At the same radiation dose, with increasing Rap concentration, the proliferation inhibition rates of the Eca109 cells were found to improve. The clone formation and survival curves of the experimental group were less than those of the control groups. Furthermore, the cell apoptosis rate and expression of cleaved caspase-3 and bax in the experimental group were higher than those of the control groups, whereas the expression of bcl-2 was less than that of the control groups. The radiation-induced DNA damage of the experimental group was greater than that of the control group. The inhibition of mTOR by Rap was found to effectively inhibit the proliferation, survival and radiation-induced DNA damage repair of the Eca109 cells following irradiation, as well as promoting radiation-induced apoptosis, thereby increasing the radiosensitivity of the esophageal carcinoma Eca109 cells.
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