ArticleContemporary oncology (Poznan, Poland)2014
Comparison of selected gene expression profiles in sensitive and resistant cancer cells treated with doxorubicin and Selol.
Article in Contemporary oncology (Poznan, Poland), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The Modulatory Effect of Selol (Se IV) on Pro-Inflammatory Pathways in RAW 264.7 Macrophages.International journal of molecular sciences · 2025Article
- Effect of Selol on Tumor Morphology and Biochemical Parameters Associated with Oxidative Stress in a Prostate Tumor-Bearing Mice Model.Nutrients · 2024Article
- Selenium-Containing Agents Acting on Cancer-A New Hope?Pharmaceutics · 2022Review
- Selenium Compounds as Novel Potential Anticancer Agents.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aim of the studyCellular resistance is strongly correlated with the risk of failure in doxorubicin (DOX) treatment, and the knowledge of the mechanisms of resistance and its possible modulation is still very limited. MATERIAL AND
methodsIn this study, we assessed the effect of 5% Selol and DOX on the expression of genes that affect cell proliferation in the resistant KB-V1 and sensitive HeLa cell lines, using RT2 ProfilerTM PCR Array matrix "Human Cancer Drug Resistance and Metabolism" (SABiosciences).
resultsWe showed that HeLa and KB-V1 cell lines, characterised by varying susceptibility to DOX, have different genetic profiles as regards the studied genes. KB-V1 cells show overexpression of MYC and BCL2 genes, which encode proteins with anti apoptotic properties. Selol, when used in KB-V1 cells, reduced the expression of MYC and BCL2 genes, suggested as a new therapeutic target in the treatment of cancers resistant to cytostatic drugs.
conclusionsThe results suggest that Selol could be used as a modulator that enhances the cytotoxic effects of doxorubicin, particularly in cells resistant to this drug.
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