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LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472

BACKGROUND: Previous studies have been reported that long non-coding RNA (lncRNA) can regulate the expression of genes which are involved in many important cellular processes The potential role of lncRNA RP11-551L14.4 in the development of breast cancer and the possible regulatory mechanisms was inv...

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Autores principales: Wang, Bin, Chen, Hang, Yang, Rui, Xing, Lei, Chen, Chuan, Chen, Junxia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: PeerJ Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745927/
https://www.ncbi.nlm.nih.gov/pubmed/36523479
http://dx.doi.org/10.7717/peerj.14482
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author Wang, Bin
Chen, Hang
Yang, Rui
Xing, Lei
Chen, Chuan
Chen, Junxia
author_facet Wang, Bin
Chen, Hang
Yang, Rui
Xing, Lei
Chen, Chuan
Chen, Junxia
author_sort Wang, Bin
collection PubMed
description BACKGROUND: Previous studies have been reported that long non-coding RNA (lncRNA) can regulate the expression of genes which are involved in many important cellular processes The potential role of lncRNA RP11-551L14.4 in the development of breast cancer and the possible regulatory mechanisms was investigated. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to analyze RP11-551L14.4 expression in 36 paired breast cancer tissues and adjacent tissues. The expression of RP11-551L14.4 in multiple breast cancer cell lines was detected by qRT-PCR. Meanwhile, overexpression of RP11-551L14.4 models was established using lentivirus in BT474 and T47D breast cancer cells. Cell counting kit-8 (CCK-8), cell colony formation and cell cycle assays were performed to detect the effects of RP11-551L14.4 on the biological function of breast cancer cells. Besides, bioinformatics techniques, dual luciferase reporter gene assay and rescue experiments were used to investigate the potential mechanisms. RESULTS: RP11-551L14.4 expression was negatively associated with the advanced tumor stage. Breast cancer patients with low RP11-551L14.4 expression manifested a poorer prognosis. The results of qRT-PCR showed that RP11-551L14.4 expression in breast cancer tissues was significantly lower than in adjacent tissues. Meanwhile, overexpression of RP11-551L14.4 significantly decreased the cell proliferation and cell cycle. Bioinformatics technology showed that RP11-551L14.4 could complementarily bind to miR-4472. qRT-PCR results indicated that the expression levels of miR-4472 and RP11-551L14.4 in breast cancer were negatively correlated. Luciferase reporter gene assay showed that miR-4472 remarkably decreased the relative luciferase activity of the wild-type RP11-551L14.4 vector. miR-4472 is a direct target gene of RP11-551L14.4. miR-4472 levels were reduced, and repulsive guidance molecule A (RGMA) mRNA or protein levels were increased after overexpression of RP11-551L14.4 in the breast cancer cells. miR-4472 reversed the effects caused by RP11-551L14.4 in breast cancer cells. CONCLUSION: RP11-551L14.4 expression was remarkably decreased in breast cancer tissues and cells. RP11-551L14.4 may inhibit the malignant progression of breast cancer by regulating miR-4472 expression.
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spelling pubmed-97459272022-12-14 LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472 Wang, Bin Chen, Hang Yang, Rui Xing, Lei Chen, Chuan Chen, Junxia PeerJ Bioinformatics BACKGROUND: Previous studies have been reported that long non-coding RNA (lncRNA) can regulate the expression of genes which are involved in many important cellular processes The potential role of lncRNA RP11-551L14.4 in the development of breast cancer and the possible regulatory mechanisms was investigated. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) was conducted to analyze RP11-551L14.4 expression in 36 paired breast cancer tissues and adjacent tissues. The expression of RP11-551L14.4 in multiple breast cancer cell lines was detected by qRT-PCR. Meanwhile, overexpression of RP11-551L14.4 models was established using lentivirus in BT474 and T47D breast cancer cells. Cell counting kit-8 (CCK-8), cell colony formation and cell cycle assays were performed to detect the effects of RP11-551L14.4 on the biological function of breast cancer cells. Besides, bioinformatics techniques, dual luciferase reporter gene assay and rescue experiments were used to investigate the potential mechanisms. RESULTS: RP11-551L14.4 expression was negatively associated with the advanced tumor stage. Breast cancer patients with low RP11-551L14.4 expression manifested a poorer prognosis. The results of qRT-PCR showed that RP11-551L14.4 expression in breast cancer tissues was significantly lower than in adjacent tissues. Meanwhile, overexpression of RP11-551L14.4 significantly decreased the cell proliferation and cell cycle. Bioinformatics technology showed that RP11-551L14.4 could complementarily bind to miR-4472. qRT-PCR results indicated that the expression levels of miR-4472 and RP11-551L14.4 in breast cancer were negatively correlated. Luciferase reporter gene assay showed that miR-4472 remarkably decreased the relative luciferase activity of the wild-type RP11-551L14.4 vector. miR-4472 is a direct target gene of RP11-551L14.4. miR-4472 levels were reduced, and repulsive guidance molecule A (RGMA) mRNA or protein levels were increased after overexpression of RP11-551L14.4 in the breast cancer cells. miR-4472 reversed the effects caused by RP11-551L14.4 in breast cancer cells. CONCLUSION: RP11-551L14.4 expression was remarkably decreased in breast cancer tissues and cells. RP11-551L14.4 may inhibit the malignant progression of breast cancer by regulating miR-4472 expression. PeerJ Inc. 2022-12-06 /pmc/articles/PMC9745927/ /pubmed/36523479 http://dx.doi.org/10.7717/peerj.14482 Text en ©2022 Wang et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, reproduction and adaptation in any medium and for any purpose provided that it is properly attributed. For attribution, the original author(s), title, publication source (PeerJ) and either DOI or URL of the article must be cited.
spellingShingle Bioinformatics
Wang, Bin
Chen, Hang
Yang, Rui
Xing, Lei
Chen, Chuan
Chen, Junxia
LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title_full LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title_fullStr LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title_full_unstemmed LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title_short LncRNA RP11-551L14.4 suppresses breast cancer development by inhibiting the expression of miR-4472
title_sort lncrna rp11-551l14.4 suppresses breast cancer development by inhibiting the expression of mir-4472
topic Bioinformatics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745927/
https://www.ncbi.nlm.nih.gov/pubmed/36523479
http://dx.doi.org/10.7717/peerj.14482
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