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Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR

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Abstract

Background

PTX is widely used in cancer treatments.

Objective

In this paper, we explored the role and potential molecular mechanism of propofol in regulating PTX sensitivity in PC cells.

Methods

Prostatic 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.

Results

PTX 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.

Conclusion

Propofol enhanced paclitaxel sensitivity in prostatic cancer cells through modulation of HOTAIR in vitro.

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Correspondence to Chunyu Gong or Jing Yang.

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Xuesong Yang, Jiao Qin, Chunyu Gong and Jing Yang declare that they have no conflict of interest.

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This study had been approved by Affiliated hospital of north sichuan medical college. No human or animal was involved in the study.

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Informed consent was obtained from all individual participants included in the study.

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Yang, X., Qin, J., Gong, C. et al. Propofol enhanced the cell sensitivity to paclitaxel (PTX) in prostatic cancer (PC) through modulation of HOTAIR. Genes Genom 43, 807–814 (2021). https://doi.org/10.1007/s13258-021-01093-0

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