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RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway

BACKGROUND: Many long noncoding RNAs (lncRNAs) are the key regulators for cancer progression, including breast cancer (BC). RUSC1 antisense 1 (RUSC1‐AS1) has been found to be highly expressed in BC, but its role and potential molecular mechanism in BC remain to be further elucidated. METHODS: Quanti...

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Autores principales: Ayoufu, Aisikeer, Paierhati, Puerkaiti, Qiao, Lei, Zhang, Nan, Abudukeremu, Muzhapaer
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10447167/
https://www.ncbi.nlm.nih.gov/pubmed/37429610
http://dx.doi.org/10.1111/1759-7714.15035
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author Ayoufu, Aisikeer
Paierhati, Puerkaiti
Qiao, Lei
Zhang, Nan
Abudukeremu, Muzhapaer
author_facet Ayoufu, Aisikeer
Paierhati, Puerkaiti
Qiao, Lei
Zhang, Nan
Abudukeremu, Muzhapaer
author_sort Ayoufu, Aisikeer
collection PubMed
description BACKGROUND: Many long noncoding RNAs (lncRNAs) are the key regulators for cancer progression, including breast cancer (BC). RUSC1 antisense 1 (RUSC1‐AS1) has been found to be highly expressed in BC, but its role and potential molecular mechanism in BC remain to be further elucidated. METHODS: Quantitative reverse transcription‐polymerase chain reaction (RT‐PCR) was utilized to measure RUSC1‐AS1, microRNA (miR)‐326 and X‐ray repair cross‐complementing group 5 (XRCC5) expression. Cell proliferation, metastasis, cell cycle, apoptosis and angiogenesis were determined by cell counting kit‐8, colony formation, transwell, flow cytometry and tube formation assays. Protein expression was detected by western blot analysis. The targeted relationship between miR‐326 and RUSC1‐AS1 or XRCC5 was validated using dual‐luciferase reporter assay and RIP assay. Xenograft models were constructed to uncover the effect of RUSC1‐AS1 on BC tumorigenesis. RESULTS: RUSC1‐AS1 was upregulated in BC, and its downregulation suppressed BC proliferation, metastasis, cell cycle, angiogenesis, and tumor growth. MiR‐326 was confirmed to be sponged by RUSC1‐AS1, and its inhibitor reversed the regulation of RUSC1‐AS1 silencing on BC progression. XRCC5 could be targeted by miR‐326. Overexpression of XRCC5 reversed the inhibitory impacts of miR‐326 on BC progression. CONCLUSION: RUSC1‐AS1 could serve as a sponge of miR‐326 to promote BC progression by targeting XRCC5, suggesting that RUSC1‐AS1 might be a target for BC treatment.
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spelling pubmed-104471672023-08-24 RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway Ayoufu, Aisikeer Paierhati, Puerkaiti Qiao, Lei Zhang, Nan Abudukeremu, Muzhapaer Thorac Cancer Original Articles BACKGROUND: Many long noncoding RNAs (lncRNAs) are the key regulators for cancer progression, including breast cancer (BC). RUSC1 antisense 1 (RUSC1‐AS1) has been found to be highly expressed in BC, but its role and potential molecular mechanism in BC remain to be further elucidated. METHODS: Quantitative reverse transcription‐polymerase chain reaction (RT‐PCR) was utilized to measure RUSC1‐AS1, microRNA (miR)‐326 and X‐ray repair cross‐complementing group 5 (XRCC5) expression. Cell proliferation, metastasis, cell cycle, apoptosis and angiogenesis were determined by cell counting kit‐8, colony formation, transwell, flow cytometry and tube formation assays. Protein expression was detected by western blot analysis. The targeted relationship between miR‐326 and RUSC1‐AS1 or XRCC5 was validated using dual‐luciferase reporter assay and RIP assay. Xenograft models were constructed to uncover the effect of RUSC1‐AS1 on BC tumorigenesis. RESULTS: RUSC1‐AS1 was upregulated in BC, and its downregulation suppressed BC proliferation, metastasis, cell cycle, angiogenesis, and tumor growth. MiR‐326 was confirmed to be sponged by RUSC1‐AS1, and its inhibitor reversed the regulation of RUSC1‐AS1 silencing on BC progression. XRCC5 could be targeted by miR‐326. Overexpression of XRCC5 reversed the inhibitory impacts of miR‐326 on BC progression. CONCLUSION: RUSC1‐AS1 could serve as a sponge of miR‐326 to promote BC progression by targeting XRCC5, suggesting that RUSC1‐AS1 might be a target for BC treatment. John Wiley & Sons Australia, Ltd 2023-07-10 /pmc/articles/PMC10447167/ /pubmed/37429610 http://dx.doi.org/10.1111/1759-7714.15035 Text en © 2023 The Authors. Thoracic Cancer published by China Lung Oncology Group and John Wiley & Sons Australia, Ltd. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 Original Articles
Ayoufu, Aisikeer
Paierhati, Puerkaiti
Qiao, Lei
Zhang, Nan
Abudukeremu, Muzhapaer
RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title_full RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title_fullStr RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title_full_unstemmed RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title_short RUSC1‐AS1 promotes the malignant progression of breast cancer depending on the regulation of the miR‐326/XRCC5 pathway
title_sort rusc1‐as1 promotes the malignant progression of breast cancer depending on the regulation of the mir‐326/xrcc5 pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10447167/
https://www.ncbi.nlm.nih.gov/pubmed/37429610
http://dx.doi.org/10.1111/1759-7714.15035
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