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Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis
Previous studies in our laboratory have reported that miR-222-3p was a tumor-suppressive miRNA in OC. This study aims to further understand the regulatory role of miR-222-3p in OC and provide a new mechanism for its prevention and treatment. We first found that miR-222-3p inhibited the migration and...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer International Publishing
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9033702/ https://www.ncbi.nlm.nih.gov/pubmed/35451651 http://dx.doi.org/10.1007/s00018-022-04250-0 |
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author | Fan, Lili Lei, Han Lin, Ying Zhou, Zhengwei Li, Juanni Wu, Anqi Shu, Guang Roger, Sébastien Yin, Gang |
author_facet | Fan, Lili Lei, Han Lin, Ying Zhou, Zhengwei Li, Juanni Wu, Anqi Shu, Guang Roger, Sébastien Yin, Gang |
author_sort | Fan, Lili |
collection | PubMed |
description | Previous studies in our laboratory have reported that miR-222-3p was a tumor-suppressive miRNA in OC. This study aims to further understand the regulatory role of miR-222-3p in OC and provide a new mechanism for its prevention and treatment. We first found that miR-222-3p inhibited the migration and proliferation of OC cells. Then, we observed CDK19 was highly expressed in OC and inversely correlated with miR-222-3p. Besides, we observed that miR-222-3p directly binds to the 3′-UTR of CDK19 and inhibits CDK19 translation, thus inhibiting OC cell migration and proliferation in vitro and repressed tumor growth in vivo. We also observed the inhibitory effect of Hotair on miR-222-3p in OC. In addition, Hotair could promote the proliferation and migration of OC cells in vitro and facilitate the growth and metastasis of tumors in vivo. Moreover, Hotair was positively correlated with CDK19 expression. These results suggest Hotair indirectly up-regulates CDK19 through sponging miR-222-3p, which enhances the malignant behavior of OC. This provides a further understanding of the mechanism of the occurrence and development of OC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00018-022-04250-0. |
format | Online Article Text |
id | pubmed-9033702 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer International Publishing |
record_format | MEDLINE/PubMed |
spelling | pubmed-90337022022-05-06 Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis Fan, Lili Lei, Han Lin, Ying Zhou, Zhengwei Li, Juanni Wu, Anqi Shu, Guang Roger, Sébastien Yin, Gang Cell Mol Life Sci Original Article Previous studies in our laboratory have reported that miR-222-3p was a tumor-suppressive miRNA in OC. This study aims to further understand the regulatory role of miR-222-3p in OC and provide a new mechanism for its prevention and treatment. We first found that miR-222-3p inhibited the migration and proliferation of OC cells. Then, we observed CDK19 was highly expressed in OC and inversely correlated with miR-222-3p. Besides, we observed that miR-222-3p directly binds to the 3′-UTR of CDK19 and inhibits CDK19 translation, thus inhibiting OC cell migration and proliferation in vitro and repressed tumor growth in vivo. We also observed the inhibitory effect of Hotair on miR-222-3p in OC. In addition, Hotair could promote the proliferation and migration of OC cells in vitro and facilitate the growth and metastasis of tumors in vivo. Moreover, Hotair was positively correlated with CDK19 expression. These results suggest Hotair indirectly up-regulates CDK19 through sponging miR-222-3p, which enhances the malignant behavior of OC. This provides a further understanding of the mechanism of the occurrence and development of OC. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00018-022-04250-0. Springer International Publishing 2022-04-22 2022 /pmc/articles/PMC9033702/ /pubmed/35451651 http://dx.doi.org/10.1007/s00018-022-04250-0 Text en © The Author(s) 2022 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/) . |
spellingShingle | Original Article Fan, Lili Lei, Han Lin, Ying Zhou, Zhengwei Li, Juanni Wu, Anqi Shu, Guang Roger, Sébastien Yin, Gang Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title | Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title_full | Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title_fullStr | Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title_full_unstemmed | Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title_short | Hotair promotes the migration and proliferation in ovarian cancer by miR-222-3p/CDK19 axis |
title_sort | hotair promotes the migration and proliferation in ovarian cancer by mir-222-3p/cdk19 axis |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9033702/ https://www.ncbi.nlm.nih.gov/pubmed/35451651 http://dx.doi.org/10.1007/s00018-022-04250-0 |
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