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Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG
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 proliferatio...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8610141/ https://www.ncbi.nlm.nih.gov/pubmed/34775376 http://dx.doi.org/10.18632/aging.203697 |
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author | Du, Xin-Tan Wang, Xiao-Yan Zheng, Ying-He Liu, Da-Peng |
author_facet | Du, Xin-Tan Wang, Xiao-Yan Zheng, Ying-He Liu, Da-Peng |
author_sort | Du, Xin-Tan |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-8610141 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Impact Journals |
record_format | MEDLINE/PubMed |
spelling | pubmed-86101412021-11-24 Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG Du, Xin-Tan Wang, Xiao-Yan Zheng, Ying-He Liu, Da-Peng Aging (Albany NY) Research Paper 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. Impact Journals 2021-11-13 /pmc/articles/PMC8610141/ /pubmed/34775376 http://dx.doi.org/10.18632/aging.203697 Text en Copyright: © 2021 Du et al. https://creativecommons.org/licenses/by/3.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Du, Xin-Tan Wang, Xiao-Yan Zheng, Ying-He Liu, Da-Peng Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title | Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title_full | Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title_fullStr | Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title_full_unstemmed | Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title_short | Propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting MIR155HG |
title_sort | propofol suppresses the growth and invasion of cervical carcinoma cells by inhibiting mir155hg |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8610141/ https://www.ncbi.nlm.nih.gov/pubmed/34775376 http://dx.doi.org/10.18632/aging.203697 |
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