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Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9

Curcumol has been reported to exert anti-tumor activity, but its intrinsic molecular mechanism in prostate cancer remains to be elucidated. The present study aimed to analyze the effect of curcumol on prostate cancer and identify its possible internal regulatory pathway using in vitro cell culture a...

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Autores principales: Sheng, Wen, Xu, Wenjing, Ding, Jin, Li, Ling, You, Xujun, Wu, Yongrong, He, Qinghu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8493056/
https://www.ncbi.nlm.nih.gov/pubmed/34590156
http://dx.doi.org/10.3892/or.2021.8197
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author Sheng, Wen
Xu, Wenjing
Ding, Jin
Li, Ling
You, Xujun
Wu, Yongrong
He, Qinghu
author_facet Sheng, Wen
Xu, Wenjing
Ding, Jin
Li, Ling
You, Xujun
Wu, Yongrong
He, Qinghu
author_sort Sheng, Wen
collection PubMed
description Curcumol has been reported to exert anti-tumor activity, but its intrinsic molecular mechanism in prostate cancer remains to be elucidated. The present study aimed to analyze the effect of curcumol on prostate cancer and identify its possible internal regulatory pathway using in vitro cell culture and in vivo tumor model experiments. The cytotoxicity of curcumol was detected using a Cell Counting Kit-8 assay and it was found that curcumol had no obvious toxicity or side effects on RWPE-1 cells. Wound healing, Transwell and flow cytometry assays demonstrated that curcumol could affect the activity of PC3 cells. The luciferase reporter assay also indicated that microRNA (miR)-9 could directly target pyruvate dehydrogenase kinase 1 (PDK1). After PC3 cells were transfected with miR-9 inhibitor or treated with curcumol, the expression levels of the PDK1/AKT/mTOR signaling pathway-related proteins [PDK1, phosphorylated (p)-AKT and p-mTOR] were increased or decreased, respectively. Next, the prostate cancer cell xenograft model was established. Tumor size and the expression levels of PDK1/AKT/mTOR signaling pathway-related factors were altered following treatment with curcumol. The in vitro and in vivo experiments collectively demonstrated that curcumol could inhibit the PDK1/AKT/mTOR signaling pathway by upregulating the expression level of miR-9. The present study found that curcumol regulates the PDK1/AKT/mTOR signaling pathway via miR-9 and affects the development of prostate cancer. These findings could provide a possible scientific insight for research into treatments for prostate cancer.
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spelling pubmed-84930562021-10-07 Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9 Sheng, Wen Xu, Wenjing Ding, Jin Li, Ling You, Xujun Wu, Yongrong He, Qinghu Oncol Rep Articles Curcumol has been reported to exert anti-tumor activity, but its intrinsic molecular mechanism in prostate cancer remains to be elucidated. The present study aimed to analyze the effect of curcumol on prostate cancer and identify its possible internal regulatory pathway using in vitro cell culture and in vivo tumor model experiments. The cytotoxicity of curcumol was detected using a Cell Counting Kit-8 assay and it was found that curcumol had no obvious toxicity or side effects on RWPE-1 cells. Wound healing, Transwell and flow cytometry assays demonstrated that curcumol could affect the activity of PC3 cells. The luciferase reporter assay also indicated that microRNA (miR)-9 could directly target pyruvate dehydrogenase kinase 1 (PDK1). After PC3 cells were transfected with miR-9 inhibitor or treated with curcumol, the expression levels of the PDK1/AKT/mTOR signaling pathway-related proteins [PDK1, phosphorylated (p)-AKT and p-mTOR] were increased or decreased, respectively. Next, the prostate cancer cell xenograft model was established. Tumor size and the expression levels of PDK1/AKT/mTOR signaling pathway-related factors were altered following treatment with curcumol. The in vitro and in vivo experiments collectively demonstrated that curcumol could inhibit the PDK1/AKT/mTOR signaling pathway by upregulating the expression level of miR-9. The present study found that curcumol regulates the PDK1/AKT/mTOR signaling pathway via miR-9 and affects the development of prostate cancer. These findings could provide a possible scientific insight for research into treatments for prostate cancer. D.A. Spandidos 2021-11 2021-09-28 /pmc/articles/PMC8493056/ /pubmed/34590156 http://dx.doi.org/10.3892/or.2021.8197 Text en Copyright: © Sheng et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Sheng, Wen
Xu, Wenjing
Ding, Jin
Li, Ling
You, Xujun
Wu, Yongrong
He, Qinghu
Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title_full Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title_fullStr Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title_full_unstemmed Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title_short Curcumol inhibits the malignant progression of prostate cancer and regulates the PDK1/AKT/mTOR pathway by targeting miR-9
title_sort curcumol inhibits the malignant progression of prostate cancer and regulates the pdk1/akt/mtor pathway by targeting mir-9
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8493056/
https://www.ncbi.nlm.nih.gov/pubmed/34590156
http://dx.doi.org/10.3892/or.2021.8197
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