ArticleTechnology in cancer research & treatment2019
Genome-Wide Profiling of the Toxic Effect of Bortezomib on Human Esophageal Carcinoma Epithelial Cells.
Article in Technology in cancer research & treatment, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 4 citations in OpenAlex.
- Identification and Verification of Ubiquitin D as a Gene Associated with Hepatitis C Virus-Induced Hepatocellular Carcinoma.Intervirology · 2022Article
- Role of HDAC6 and Its Selective Inhibitors in Gastrointestinal Cancer.Frontiers in cell and developmental biology · 2021Review
- Protein Kinase D 1 Predicts Poor Treatment Response and Unfavorable Survival of Bortezomib-Based Treatment, and Its Knockdown Enhances Drug Sensitivity to Bortezomib in Multiple Myeloma.Technology in cancer research & treatmentArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesBortezomib has been widely used to treat multiple myeloma and other hematological malignancies. However, not much is known about its effect on solid tumors. The aim of this study was to study the effect of Bortezomib on human esophageal cancer cell lines and investigate the potential target pathways.
methodsTwo human esophageal cancer cell lines, TE-1 and KYSE-150, were used in this study. Cell viability, cell cycle distribution, and apoptosis after Bortezomib treatment was detected by Cell Counting Kit-8, flow cytometry, and Annexin V/propidium iodide staining, respectively. The genes targeted by Bortezomib were analyzed at the messenger RNA level by microarray chips and quantitative real-time polymerase chain reaction.
resultsThe proliferation of human esophageal cancer cell lines was inhibited by Bortezomib in a dose- and time-dependent manner. Bortezomib treatment led to G
conclusionBortezomib could suppress cell viability, cause G
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Registered trials
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