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A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis

OBJECTIVE: Compelling evidence suggested that lncRNAs performed vital functions in the development of breast cancer (BC). The study intended to mine the functional roles of LINC01574 in BC and further excavated its underlying regulatory mechanism. METHODS: The expression and prognosis of LINC01574 i...

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Autores principales: Zhang, Liang, Wu, Lingyuan, Wei, Mengjiao, Ding, Peikai, Tian, Xingsong, Zhu, Kunbing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9348968/
https://www.ncbi.nlm.nih.gov/pubmed/35935583
http://dx.doi.org/10.1155/2022/4201283
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author Zhang, Liang
Wu, Lingyuan
Wei, Mengjiao
Ding, Peikai
Tian, Xingsong
Zhu, Kunbing
author_facet Zhang, Liang
Wu, Lingyuan
Wei, Mengjiao
Ding, Peikai
Tian, Xingsong
Zhu, Kunbing
author_sort Zhang, Liang
collection PubMed
description OBJECTIVE: Compelling evidence suggested that lncRNAs performed vital functions in the development of breast cancer (BC). The study intended to mine the functional roles of LINC01574 in BC and further excavated its underlying regulatory mechanism. METHODS: The expression and prognosis of LINC01574 in BC were detected by integrating analysis of data mining, bioinformatics, and RT-qPCR. Then, the effect of LINC01574 knockdown on BC cell growth and metastasis was evaluated in vitro and in vivo. Interactions between miR-6745 and LINC01574 or TTYH3 were revealed by both target prediction and dual luciferase reporter assay. RESULTS: Our data found that LINC01574 was markedly elevated in BC tissues and cells and was an independent prognostic risk factor for patients with BC. Further functional studies revealed that knockdown of LINC01574 remarkably inhibited the growth and metastasis of BC cells in vitro and in vivo. Mechanistically, LINC01574 competitively binds with miR-6745 to prevent the degradation of TTYH3, thereby promoting the development of BC. CONCLUSION: Our results unmasked a novel LINC01574/miR-6745/TTYH3 regulatory axis in BC progression and suggested that LINC01574 might be a promising prognostic indicator and therapeutic target for patients with BC.
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spelling pubmed-93489682022-08-04 A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis Zhang, Liang Wu, Lingyuan Wei, Mengjiao Ding, Peikai Tian, Xingsong Zhu, Kunbing J Immunol Res Research Article OBJECTIVE: Compelling evidence suggested that lncRNAs performed vital functions in the development of breast cancer (BC). The study intended to mine the functional roles of LINC01574 in BC and further excavated its underlying regulatory mechanism. METHODS: The expression and prognosis of LINC01574 in BC were detected by integrating analysis of data mining, bioinformatics, and RT-qPCR. Then, the effect of LINC01574 knockdown on BC cell growth and metastasis was evaluated in vitro and in vivo. Interactions between miR-6745 and LINC01574 or TTYH3 were revealed by both target prediction and dual luciferase reporter assay. RESULTS: Our data found that LINC01574 was markedly elevated in BC tissues and cells and was an independent prognostic risk factor for patients with BC. Further functional studies revealed that knockdown of LINC01574 remarkably inhibited the growth and metastasis of BC cells in vitro and in vivo. Mechanistically, LINC01574 competitively binds with miR-6745 to prevent the degradation of TTYH3, thereby promoting the development of BC. CONCLUSION: Our results unmasked a novel LINC01574/miR-6745/TTYH3 regulatory axis in BC progression and suggested that LINC01574 might be a promising prognostic indicator and therapeutic target for patients with BC. Hindawi 2022-07-27 /pmc/articles/PMC9348968/ /pubmed/35935583 http://dx.doi.org/10.1155/2022/4201283 Text en Copyright © 2022 Liang Zhang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Zhang, Liang
Wu, Lingyuan
Wei, Mengjiao
Ding, Peikai
Tian, Xingsong
Zhu, Kunbing
A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title_full A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title_fullStr A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title_full_unstemmed A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title_short A Novel Identified Long Intergenic Noncoding RNA, LINC01574, Contributes to Breast Cancer Deterioration via the Regulation of miR-6745/TTYH3 Axis
title_sort novel identified long intergenic noncoding rna, linc01574, contributes to breast cancer deterioration via the regulation of mir-6745/ttyh3 axis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9348968/
https://www.ncbi.nlm.nih.gov/pubmed/35935583
http://dx.doi.org/10.1155/2022/4201283
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