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CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity
BACKGROUND: Ovarian cancer recurrence and chemotherapy resistance are still urgent issues, and exploring the mechanisms of metastasis and chemotherapy resistance is beneficial to the development of therapeutic methods. Caspase recruitment domain family member 9 (CARD9) and homeobox B5 (HOXB5) are re...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703781/ https://www.ncbi.nlm.nih.gov/pubmed/36443670 http://dx.doi.org/10.1186/s12860-022-00447-0 |
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author | Wang, Yanming Wang, Chao Zhu, Yan |
author_facet | Wang, Yanming Wang, Chao Zhu, Yan |
author_sort | Wang, Yanming |
collection | PubMed |
description | BACKGROUND: Ovarian cancer recurrence and chemotherapy resistance are still urgent issues, and exploring the mechanisms of metastasis and chemotherapy resistance is beneficial to the development of therapeutic methods. Caspase recruitment domain family member 9 (CARD9) and homeobox B5 (HOXB5) are related and both are upregulated in ovarian cancer. This study aimed to define their functions in ovarian cancer cell proliferation, migration, and cisplatin sensitivity. RESULTS: The levels of CARD9 were detected in acquired ovarian cancer tissues and cell lines. CARD9 was indeed abnormally upregulated in them. CARD9 knockdown significantly suppressed cell proliferation, colony formation, migration, cycle arrest, and cisplatin sensitivity. HOXB5 bound to the CARD9 promoter, and HOXB5 overexpression reversed the regulation by CARD9 knockdown in cells, as well as the activation of NF-κB signaling. This indicated that CARD9 was positively regulated by HOXB5 in ovarian cancer cells. CONCLUSION: Together, CARD9 is involved in ovarian cancer cell proliferation, migration, and cisplatin sensitivity via NF-κB signaling after transcriptional activation by HOXB5. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12860-022-00447-0. |
format | Online Article Text |
id | pubmed-9703781 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-97037812022-11-29 CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity Wang, Yanming Wang, Chao Zhu, Yan BMC Mol Cell Biol Research BACKGROUND: Ovarian cancer recurrence and chemotherapy resistance are still urgent issues, and exploring the mechanisms of metastasis and chemotherapy resistance is beneficial to the development of therapeutic methods. Caspase recruitment domain family member 9 (CARD9) and homeobox B5 (HOXB5) are related and both are upregulated in ovarian cancer. This study aimed to define their functions in ovarian cancer cell proliferation, migration, and cisplatin sensitivity. RESULTS: The levels of CARD9 were detected in acquired ovarian cancer tissues and cell lines. CARD9 was indeed abnormally upregulated in them. CARD9 knockdown significantly suppressed cell proliferation, colony formation, migration, cycle arrest, and cisplatin sensitivity. HOXB5 bound to the CARD9 promoter, and HOXB5 overexpression reversed the regulation by CARD9 knockdown in cells, as well as the activation of NF-κB signaling. This indicated that CARD9 was positively regulated by HOXB5 in ovarian cancer cells. CONCLUSION: Together, CARD9 is involved in ovarian cancer cell proliferation, migration, and cisplatin sensitivity via NF-κB signaling after transcriptional activation by HOXB5. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12860-022-00447-0. BioMed Central 2022-11-28 /pmc/articles/PMC9703781/ /pubmed/36443670 http://dx.doi.org/10.1186/s12860-022-00447-0 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/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Wang, Yanming Wang, Chao Zhu, Yan CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title | CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title_full | CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title_fullStr | CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title_full_unstemmed | CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title_short | CARD9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
title_sort | card9 contributes to ovarian cancer cell proliferation, cycle arrest, and cisplatin sensitivity |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9703781/ https://www.ncbi.nlm.nih.gov/pubmed/36443670 http://dx.doi.org/10.1186/s12860-022-00447-0 |
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