Research Paper Volume 13, Issue 21 pp 24464—24475
Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG
- 1 Department of Anesthesia and Perioperative Medicine, Zaozhuang Municipal Hospital, Zaozhuang, Shandong, People’s Republic of China
- 2 Department of Gynecology and Obstetrics, Zaozhuang Hospital, Zaozhuang Mining Group, Zaozhuang, Shandong, People’s Republic of China
- 3 Department of Anesthesiology, Zaozhuang Hospital, Zaozhuang Mining Group, Zaozhuang, Shandong, People’s Republic of China
Received: June 25, 2021 Accepted: October 26, 2021 Published: November 13, 2021https://doi.org/10.18632/aging.203697
How to Cite
Copyright: © 2021 Du et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Background: Cervical cancer is the most prevalent malignancy worldwide and propofol reportedly has anti-cancer efficiencies. Herein, we tried to address the potential anti-cancer effects of propofol in cervical carcinoma.
Materials and Methods: The suppression effects of propofol on the proliferation and invasion of cervical cancer cells were analyzed by Cell Counting Kit-8 (CCK-8), colony formation and Transwell invasion assay. The protein expressions of epithelial marker, E-cadherin and mesenchymal marker, N-cadherin were evaluated using western blot. The level of MIR155 host gene (MIR155HG) was determined by qRT-PCR assay. The anti-cancer impact of propofol on cervical cancer cells growth in vivo was determined by means of xenograft tumor model and lung metastasis model.
Results: In vitro, propofol inhibited the growth and colony-formation of cervical carcinoma cells. Meanwhile, propofol treatment reduced the invasive trait of cervical carcinoma cells. In addition, MIR155HG was identified to be distinctly upregulated in cervical carcinoma when compared within normal. Propofol treatment decreased the expression of MIR155HG in cervical cancer cells. Consistently, the results from in vivo xenograft model indicated that propofol repressed cervical cancer cells growth and decreased the expression of MIR155HG in vivo. Furthermore, reintroduction of MIR155HG into cervical cancer cells counteracted the inhibitory potency of propofol on the growth and aggressive phenotypes in cervical carcinoma cells.
Conclusions: Altogether, these results indicated that propofol restrained the growth and invasion of cervical cancer cells partly via regulating MIR155HG expression.