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The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro

BACKGROUND: Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. METHODS: Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was...

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Autores principales: Li, Huiqing, Ma, Zhenzhen, Lei, Yunlong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404350/
https://www.ncbi.nlm.nih.gov/pubmed/34461834
http://dx.doi.org/10.1186/s12871-021-01429-z
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author Li, Huiqing
Ma, Zhenzhen
Lei, Yunlong
author_facet Li, Huiqing
Ma, Zhenzhen
Lei, Yunlong
author_sort Li, Huiqing
collection PubMed
description BACKGROUND: Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. METHODS: Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively. RESULTS: Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death. CONCLUSIONS: Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition.
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spelling pubmed-84043502021-08-31 The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro Li, Huiqing Ma, Zhenzhen Lei, Yunlong BMC Anesthesiol Research Article BACKGROUND: Opioid receptors are implicated in cell proliferation and cancer migration. However, the effects and underlying mechanisms of opioid receptor κ (OPRK1) in breast cancer remain unknown. METHODS: Small interfering RNA (siRNAs) was used to knockdown the expression of OPRK1. Western blot was used to determine the protein expression and reverse transcription-quantitative PCR (RT-qPCR) determined the genes transcription. Cell viability was detected by MTT assay and cell death rates were determined by Annexin V/PI and flow cytometry. Cell migration and invasion were detected by wound healing analysis and transwell assay, respectively. RESULTS: Our research demonstrated that OPRK1 was overexpressed in breast cancer cells compared with the normal human mammary epithelial cells. OPRK1 knockdown could inhibited cell viability and migration in cancer cells, accompanied with the decreased proteins and genes expression of N-cadherin, Snail, MMP2 and Vimentin, while the E-cadherin expression was increased. Additionally, OPRK1 knockdown also promoted PI3K/AKT signaling inactivation. Activation of AKT reversed the OPRK1 knockdown-induced cell viability inhibition and migration suppression, while inhibition of AKT reduced cell viability and promoted cell death. CONCLUSIONS: Our findings illustrated the role of OPRK1 played on promoting migration in vitro, and we also provided the therapeutic research of OPRK1 knockdown combined with AKT inhibition. BioMed Central 2021-08-30 /pmc/articles/PMC8404350/ /pubmed/34461834 http://dx.doi.org/10.1186/s12871-021-01429-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Li, Huiqing
Ma, Zhenzhen
Lei, Yunlong
The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title_full The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title_fullStr The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title_full_unstemmed The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title_short The expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
title_sort expression of kappa-opioid receptor promotes the migration of breast cancer cells in vitro
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8404350/
https://www.ncbi.nlm.nih.gov/pubmed/34461834
http://dx.doi.org/10.1186/s12871-021-01429-z
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