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miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway
AIM: Aberrantly expressed microRNAs (miRNAs) are involved in many diseases including cancer. The expression of miR-15a was reported to be downregulated in papillary thyroid carcinoma (PTC) compared to control tissue. However, the mechanism underlying this downregulation remains unclear. METHODS: The...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689766/ https://www.ncbi.nlm.nih.gov/pubmed/31496725 http://dx.doi.org/10.2147/OTT.S213210 |
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author | Jin, Jin Zhang, Jie Xue, Yigui Luo, Li Wang, Siyao Tian, Haoming |
author_facet | Jin, Jin Zhang, Jie Xue, Yigui Luo, Li Wang, Siyao Tian, Haoming |
author_sort | Jin, Jin |
collection | PubMed |
description | AIM: Aberrantly expressed microRNAs (miRNAs) are involved in many diseases including cancer. The expression of miR-15a was reported to be downregulated in papillary thyroid carcinoma (PTC) compared to control tissue. However, the mechanism underlying this downregulation remains unclear. METHODS: The effects of miR-15a on the proliferation and invasion of PTC cells were evaluated by CCK-8 and transwell assays, respectively. Expression levels of AKT and rearranged during transfection (RET) in cells were assessed using Western blotting. The correlation of RET and miR-15a was validated by luciferase reporter assay. Moreover, in vivo assay was performed to demonstrate the effect of miR-15a on tumor growth. RESULTS: We confirmed that the expression of miR-15a was significantly lower in PTC tissue than that in normal tissue. Overexpression of miR-15a notably inhibited PTC cell proliferation and invasion via promoting apoptosis. Additionally, RET was found to be a target of miR-15a and this correlation was confirmed by dual-luciferase assay and Western blot. Furthermore, in vivo study revealed that overexpression of miR-15a inhibited tumor growth via downregulating the levels of RET and phosphorylated AKT. CONCLUSION: In the present study, we demonstrated that miR-15a played an antitumor role in regulating PTC via targeting RET/AKT pathway. Therefore, miR-15a may serve as a potential molecular target for the treatment of PTC. |
format | Online Article Text |
id | pubmed-6689766 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-66897662019-09-06 miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway Jin, Jin Zhang, Jie Xue, Yigui Luo, Li Wang, Siyao Tian, Haoming Onco Targets Ther Original Research AIM: Aberrantly expressed microRNAs (miRNAs) are involved in many diseases including cancer. The expression of miR-15a was reported to be downregulated in papillary thyroid carcinoma (PTC) compared to control tissue. However, the mechanism underlying this downregulation remains unclear. METHODS: The effects of miR-15a on the proliferation and invasion of PTC cells were evaluated by CCK-8 and transwell assays, respectively. Expression levels of AKT and rearranged during transfection (RET) in cells were assessed using Western blotting. The correlation of RET and miR-15a was validated by luciferase reporter assay. Moreover, in vivo assay was performed to demonstrate the effect of miR-15a on tumor growth. RESULTS: We confirmed that the expression of miR-15a was significantly lower in PTC tissue than that in normal tissue. Overexpression of miR-15a notably inhibited PTC cell proliferation and invasion via promoting apoptosis. Additionally, RET was found to be a target of miR-15a and this correlation was confirmed by dual-luciferase assay and Western blot. Furthermore, in vivo study revealed that overexpression of miR-15a inhibited tumor growth via downregulating the levels of RET and phosphorylated AKT. CONCLUSION: In the present study, we demonstrated that miR-15a played an antitumor role in regulating PTC via targeting RET/AKT pathway. Therefore, miR-15a may serve as a potential molecular target for the treatment of PTC. Dove 2019-08-06 /pmc/articles/PMC6689766/ /pubmed/31496725 http://dx.doi.org/10.2147/OTT.S213210 Text en © 2019 Jin et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Jin, Jin Zhang, Jie Xue, Yigui Luo, Li Wang, Siyao Tian, Haoming miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title | miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title_full | miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title_fullStr | miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title_full_unstemmed | miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title_short | miRNA-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating AKT pathway |
title_sort | mirna-15a regulates the proliferation and apoptosis of papillary thyroid carcinoma via regulating akt pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689766/ https://www.ncbi.nlm.nih.gov/pubmed/31496725 http://dx.doi.org/10.2147/OTT.S213210 |
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