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CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis

BACKGROUND: Breast cancer (BC) poses serious threats to women’s health. A large number of reports have proved that circular RNAs (circRNAs) exert vital functions in human cancers, including BC. METHODS: The function of circPDSS1 in BC cells was tested by CCK-8, colony formation, TUNEL, transwell-inv...

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Autores principales: Liu, Xia, Song, Jingyong, Kang, Yu, Wang, Yaojia, Chen, Anyue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9331068/
https://www.ncbi.nlm.nih.gov/pubmed/35902921
http://dx.doi.org/10.1186/s12935-022-02657-0
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author Liu, Xia
Song, Jingyong
Kang, Yu
Wang, Yaojia
Chen, Anyue
author_facet Liu, Xia
Song, Jingyong
Kang, Yu
Wang, Yaojia
Chen, Anyue
author_sort Liu, Xia
collection PubMed
description BACKGROUND: Breast cancer (BC) poses serious threats to women’s health. A large number of reports have proved that circular RNAs (circRNAs) exert vital functions in human cancers, including BC. METHODS: The function of circPDSS1 in BC cells was tested by CCK-8, colony formation, TUNEL, transwell-invasion, wound healing, and IF assays. RNA pull down, luciferase reporter and RIP assays were employed to verify the relationship among circPDSS1, miR-320c and CKAP5. RESULTS: CircPDSS1 was upregulated in BC cells, and circPDSS1 knockdown repressed BC cell malignant behaviors. Further, circPDSS1 was found to bind to miR-320c in BC cells, and miR-320c overexpression suppressed malignant processes of BC cells. MiR-320c could also bind to CKAP5. Moreover, miR-320c inhibition increased the level of CKAP5, but circPDSS1 downregulation decreased the level of CKAP5. Finally, rescue experiments indicated that CKAP5 knockdown countervailed the promoting effect of miR-320c inhibition on the malignant behaviors of circPDSS1-depleted BC cells. CONCLUSIONS: CircPDSS1 promotes proliferation, invasion, migration as well as EMT of BC cells by modulating miR-320c/CKAP5 axis. Our finding may be useful for researchers to find new potential therapeutic or diagnostic targets for BC.
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spelling pubmed-93310682022-07-29 CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis Liu, Xia Song, Jingyong Kang, Yu Wang, Yaojia Chen, Anyue Cancer Cell Int Research BACKGROUND: Breast cancer (BC) poses serious threats to women’s health. A large number of reports have proved that circular RNAs (circRNAs) exert vital functions in human cancers, including BC. METHODS: The function of circPDSS1 in BC cells was tested by CCK-8, colony formation, TUNEL, transwell-invasion, wound healing, and IF assays. RNA pull down, luciferase reporter and RIP assays were employed to verify the relationship among circPDSS1, miR-320c and CKAP5. RESULTS: CircPDSS1 was upregulated in BC cells, and circPDSS1 knockdown repressed BC cell malignant behaviors. Further, circPDSS1 was found to bind to miR-320c in BC cells, and miR-320c overexpression suppressed malignant processes of BC cells. MiR-320c could also bind to CKAP5. Moreover, miR-320c inhibition increased the level of CKAP5, but circPDSS1 downregulation decreased the level of CKAP5. Finally, rescue experiments indicated that CKAP5 knockdown countervailed the promoting effect of miR-320c inhibition on the malignant behaviors of circPDSS1-depleted BC cells. CONCLUSIONS: CircPDSS1 promotes proliferation, invasion, migration as well as EMT of BC cells by modulating miR-320c/CKAP5 axis. Our finding may be useful for researchers to find new potential therapeutic or diagnostic targets for BC. BioMed Central 2022-07-28 /pmc/articles/PMC9331068/ /pubmed/35902921 http://dx.doi.org/10.1186/s12935-022-02657-0 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
Liu, Xia
Song, Jingyong
Kang, Yu
Wang, Yaojia
Chen, Anyue
CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title_full CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title_fullStr CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title_full_unstemmed CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title_short CircPDSS1 promotes the proliferation, invasion, migration, and EMT of breast cancer cell via regulating miR-320c/CKAP5 axis
title_sort circpdss1 promotes the proliferation, invasion, migration, and emt of breast cancer cell via regulating mir-320c/ckap5 axis
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9331068/
https://www.ncbi.nlm.nih.gov/pubmed/35902921
http://dx.doi.org/10.1186/s12935-022-02657-0
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