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MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway
BACKGROUND: Cervical cancer (CC) is frequently diagnosed, and accounts for a large proportion of cancer-related mortality worldwide. Therefore, it is an urgent need to explore the mechanisms of CC progression and seek new therapeutic targets. We know that microRNA-137 (miR-137) is involved in CC pro...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799131/ https://www.ncbi.nlm.nih.gov/pubmed/35116675 http://dx.doi.org/10.21037/tcr-21-1049 |
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author | Gui, Ying Wang, Lina Huang, Zhihong |
author_facet | Gui, Ying Wang, Lina Huang, Zhihong |
author_sort | Gui, Ying |
collection | PubMed |
description | BACKGROUND: Cervical cancer (CC) is frequently diagnosed, and accounts for a large proportion of cancer-related mortality worldwide. Therefore, it is an urgent need to explore the mechanisms of CC progression and seek new therapeutic targets. We know that microRNA-137 (miR-137) is involved in CC progression; however, it’s mechanism in CC has not yet been clarified. METHODS: Quantitative real-time PCR (qRT-PCR) was applied to detect the expressions of miR-137 and Notch homolog 1 messenger RNA (Notch1 mRNA) in CC cells. Cell Counting Kit-8 (CCK-8) and Transwell assay were utilized to monitor the proliferation, invasion, and migration of CC cells. The binding relationship of miR-137 with Notch1 was detected by dual luciferase reporter gene assay. Western blot was used to determine the expressions of Notch1, p-AKT/AKT, and p-mTOR/mTOR signaling pathways. RESULTS: The results showed that miR-137 was down-regulated and Notch1 was up-regulated in CC cells. MiR-137 was reversely correlated with Notch1, and Notch1 partially reversed the promotion of miR-137 silencing on malignant phenotype of CC cells. Furthermore, in vitro experiments confirmed that miR-137 partially impeded CC progression via regulation of the Notch1 and PI3K/AKT/mTOR axis. CONCLUSIONS: MiR-137 targets Notch1 and regulates CC through the PI3K/Akt/mTOR pathway. The miR-137/Notch1 axis may be a promising target for CC patients, and these findings can provide a reference for the clinical treatment of CC. |
format | Online Article Text |
id | pubmed-8799131 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87991312022-02-02 MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway Gui, Ying Wang, Lina Huang, Zhihong Transl Cancer Res Original Article BACKGROUND: Cervical cancer (CC) is frequently diagnosed, and accounts for a large proportion of cancer-related mortality worldwide. Therefore, it is an urgent need to explore the mechanisms of CC progression and seek new therapeutic targets. We know that microRNA-137 (miR-137) is involved in CC progression; however, it’s mechanism in CC has not yet been clarified. METHODS: Quantitative real-time PCR (qRT-PCR) was applied to detect the expressions of miR-137 and Notch homolog 1 messenger RNA (Notch1 mRNA) in CC cells. Cell Counting Kit-8 (CCK-8) and Transwell assay were utilized to monitor the proliferation, invasion, and migration of CC cells. The binding relationship of miR-137 with Notch1 was detected by dual luciferase reporter gene assay. Western blot was used to determine the expressions of Notch1, p-AKT/AKT, and p-mTOR/mTOR signaling pathways. RESULTS: The results showed that miR-137 was down-regulated and Notch1 was up-regulated in CC cells. MiR-137 was reversely correlated with Notch1, and Notch1 partially reversed the promotion of miR-137 silencing on malignant phenotype of CC cells. Furthermore, in vitro experiments confirmed that miR-137 partially impeded CC progression via regulation of the Notch1 and PI3K/AKT/mTOR axis. CONCLUSIONS: MiR-137 targets Notch1 and regulates CC through the PI3K/Akt/mTOR pathway. The miR-137/Notch1 axis may be a promising target for CC patients, and these findings can provide a reference for the clinical treatment of CC. AME Publishing Company 2021-08 /pmc/articles/PMC8799131/ /pubmed/35116675 http://dx.doi.org/10.21037/tcr-21-1049 Text en 2021 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/. |
spellingShingle | Original Article Gui, Ying Wang, Lina Huang, Zhihong MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title | MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title_full | MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title_fullStr | MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title_full_unstemmed | MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title_short | MiR-137 inhibits cervical cancer progression via down-modulating Notch1 and inhibiting the PI3K/AKT/mTOR signaling pathway |
title_sort | mir-137 inhibits cervical cancer progression via down-modulating notch1 and inhibiting the pi3k/akt/mtor signaling pathway |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799131/ https://www.ncbi.nlm.nih.gov/pubmed/35116675 http://dx.doi.org/10.21037/tcr-21-1049 |
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