ArticleGenes & genomics2021
Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR.
Article in Genes & genomics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- HOTAIR in cancer: diagnostic, prognostic, and therapeutic perspectives.Cancer cell international · 2024Review
- lncRNA HOTAIR and Cardiovascular diseases.Functional & integrative genomics · 2024Review
- The effect of propofol on chemosensitivity of paclitaxel in cervical cancer cells.Cancer medicine · 2023Article
- Review
- AS-IV enhances the antitumor effects of propofol in NSCLC cells by inhibiting autophagy.Open medicine (Warsaw, Poland) · 2023Article
- Functions and underlying mechanisms of lncRNA HOTAIR in cancer chemotherapy resistance.Cell death discovery · 2022Review
- An intravenous anesthetic drug-propofol, influences the biological characteristics of malignant tumors and reshapes the tumor microenvironment: A narrative literature review.Frontiers in pharmacology · 2022Review
- Folic Acid-Modified miR-491-5p-Loaded ZIF-8 Nanoparticles Inhibit Castration-Resistant Prostate Cancer by Regulating the Expression of EPHX1.Frontiers in bioengineering and biotechnology · 2021Article
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
backgroundPTX is widely used in cancer treatments.
objectiveIn this paper, we explored the role and potential molecular mechanism of propofol in regulating PTX sensitivity in PC cells.
methodsProstatic cancer cell line PC3 was treated using different concentrations of PTX (10 nM, 50 nM), propofol (150 μM, 300 μM) or transfected with overexpressed HOTAIR plasmid. HOTAIR expression was analyzed by RT-qPCR. Apoptosis of PC3 cells was observed by flow cytometry method while cell viability was evaluated by CCK-8. Moreover, apoptosis-related genes, Bcl-2 and Bax were detected by Western blot methods. E-cadherin, N-cadherin and Vimentin protein concentrations were monitored by ELISA.
resultsPTX significantly increased apoptosis of PC3 cells and reduced cell viability in a dose-dependent manner. Moreover, Protein expression of Bcl-2 was obviously inhibited while Bax protein expression level was provoked. Furthermore, E-cadherin protein concentration increased while N-cadherin and Vimentin decreased due to increasing PTX treatments. HOTAIR expression dropped due to PTX treatment while overexpression of HOTAIR induced cell viability, EMT and deterred apoptosis. Propofol ignited the PTX function while upregulation of HOTAIR partially reversed this.
conclusionPropofol enhanced paclitaxel sensitivity in prostatic cancer cells through modulation of HOTAIR in vitro.
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