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hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway

Oral cancer is one of the leading causes of death worldwide, with a reported 5-year survival rate of ~50% after treatment. The treatment measures for oral cancer are very expensive and affordability is low. Thus, it is necessary to develop more effective therapies to treat oral cancer. A number of s...

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Autores principales: Wang, Yifan, Liu, Shanshan, Lv, Feifei, Zhai, Wenjing, Wang, Weina, Duan, Yanhao, Qiu, Yongle
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206674/
https://www.ncbi.nlm.nih.gov/pubmed/37203400
http://dx.doi.org/10.3892/mmr.2023.13015
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author Wang, Yifan
Liu, Shanshan
Lv, Feifei
Zhai, Wenjing
Wang, Weina
Duan, Yanhao
Qiu, Yongle
author_facet Wang, Yifan
Liu, Shanshan
Lv, Feifei
Zhai, Wenjing
Wang, Weina
Duan, Yanhao
Qiu, Yongle
author_sort Wang, Yifan
collection PubMed
description Oral cancer is one of the leading causes of death worldwide, with a reported 5-year survival rate of ~50% after treatment. The treatment measures for oral cancer are very expensive and affordability is low. Thus, it is necessary to develop more effective therapies to treat oral cancer. A number of studies have found that miRNAs are invasive biomarkers and have therapeutic potential in a variety of cancers. The present study included 30 oral patients and 30 healthy controls. Clinicopathological characteristic and miR-216a-3p/β-catenin expression level of 30 oral cancer patients were analyzed. In addition, two oral cancer cell lines (HSC-6 and CAL-27) were used for mechanism-of-action study. The expression level of miR-216a-3p was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage. Inhibition of miR-216a-3p potently suppressed cell viability and induced apoptosis of oral cancer cells. It was found that effects of miR-216a-3p on oral cancer were through Wnt3a signaling. It was also found that the expression level of β-catenin was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage; the effects of miR-216a-3p on oral cancer were through β-catenin. In conclusion, miR-216a-3p and the Wnt-β-catenin signaling pathway may be interesting candidates to develop effective therapies for oral cancers.
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spelling pubmed-102066742023-05-25 hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway Wang, Yifan Liu, Shanshan Lv, Feifei Zhai, Wenjing Wang, Weina Duan, Yanhao Qiu, Yongle Mol Med Rep Articles Oral cancer is one of the leading causes of death worldwide, with a reported 5-year survival rate of ~50% after treatment. The treatment measures for oral cancer are very expensive and affordability is low. Thus, it is necessary to develop more effective therapies to treat oral cancer. A number of studies have found that miRNAs are invasive biomarkers and have therapeutic potential in a variety of cancers. The present study included 30 oral patients and 30 healthy controls. Clinicopathological characteristic and miR-216a-3p/β-catenin expression level of 30 oral cancer patients were analyzed. In addition, two oral cancer cell lines (HSC-6 and CAL-27) were used for mechanism-of-action study. The expression level of miR-216a-3p was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage. Inhibition of miR-216a-3p potently suppressed cell viability and induced apoptosis of oral cancer cells. It was found that effects of miR-216a-3p on oral cancer were through Wnt3a signaling. It was also found that the expression level of β-catenin was higher in oral cancer patients compared with healthy controls and positively associated with tumor stage; the effects of miR-216a-3p on oral cancer were through β-catenin. In conclusion, miR-216a-3p and the Wnt-β-catenin signaling pathway may be interesting candidates to develop effective therapies for oral cancers. D.A. Spandidos 2023-05-16 /pmc/articles/PMC10206674/ /pubmed/37203400 http://dx.doi.org/10.3892/mmr.2023.13015 Text en Copyright: © Wang 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
Wang, Yifan
Liu, Shanshan
Lv, Feifei
Zhai, Wenjing
Wang, Weina
Duan, Yanhao
Qiu, Yongle
hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title_full hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title_fullStr hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title_full_unstemmed hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title_short hsa‑miR‑216a‑3p regulates cell proliferation in oral cancer via the Wnt3a/β‑catenin pathway
title_sort hsa‑mir‑216a‑3p regulates cell proliferation in oral cancer via the wnt3a/β‑catenin pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10206674/
https://www.ncbi.nlm.nih.gov/pubmed/37203400
http://dx.doi.org/10.3892/mmr.2023.13015
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