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Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)

BACKGROUND: Long non-coding RNA PCAT7 has been revealed to participate in tumorigenesis of various cancers. However, the mechanism of PCAT7 in non-small cell lung cancer (NSCLC) has not been identified. Hence, this study aimed to determine the function of PCAT7 in NSCLC. MATERIAL/METHODS: The expres...

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Autores principales: Liu, Qiongliang, Wu, Yingying, Xiao, Jie, Zou, Jianyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749158/
https://www.ncbi.nlm.nih.gov/pubmed/29275424
http://dx.doi.org/10.12659/MSM.907904
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author Liu, Qiongliang
Wu, Yingying
Xiao, Jie
Zou, Jianyong
author_facet Liu, Qiongliang
Wu, Yingying
Xiao, Jie
Zou, Jianyong
author_sort Liu, Qiongliang
collection PubMed
description BACKGROUND: Long non-coding RNA PCAT7 has been revealed to participate in tumorigenesis of various cancers. However, the mechanism of PCAT7 in non-small cell lung cancer (NSCLC) has not been identified. Hence, this study aimed to determine the function of PCAT7 in NSCLC. MATERIAL/METHODS: The expression level of PCAT7 in 96 pairs of NSCLC tissues and 6 cell lines was detected by qRT-PCR. Proliferation assay, flow cytometric analysis, transwell/migration assay, and Western blotting assay were performed to detect the relation between PCAT7 and malignant behaviors of NSCLC cells in vitro, including cell proliferation, apoptosis, migration, invasion, and epithelial-to-mesenchymal transition (EMT). Rescue assays were carried out to confirm the contribution of PCAT7 to the progression of NSCLC cells by targeting miR-134-5p. RESULTS: PCAT7 was found to be overexpressed in NSCLC tissues (compared with corresponding non-tumor tissues) and NSCLC cells (compared with normal cell line 16-HBE). Overexpression of PCAT7 resulted in the promotion of tumor cell proliferation, inhibition of cells apoptosis, facilitation of cells metastasis, and formation of EMT phenotype, while PCAT7 expression deletion remarkably prohibited cell proliferation, accelerated their apoptosis, weakened metastasis, and reversed EMT to MET. miR-134-5P, as a target gene of PCAT7, restored the effects of down-regulation of PCAT7. CONCLUSIONS: These findings demonstrate that PCAT7 participates in tumor progression in NSCLC by inhibiting miR-134-5p.
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spelling pubmed-57491582018-01-05 Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC) Liu, Qiongliang Wu, Yingying Xiao, Jie Zou, Jianyong Med Sci Monit Lab/In Vitro Research BACKGROUND: Long non-coding RNA PCAT7 has been revealed to participate in tumorigenesis of various cancers. However, the mechanism of PCAT7 in non-small cell lung cancer (NSCLC) has not been identified. Hence, this study aimed to determine the function of PCAT7 in NSCLC. MATERIAL/METHODS: The expression level of PCAT7 in 96 pairs of NSCLC tissues and 6 cell lines was detected by qRT-PCR. Proliferation assay, flow cytometric analysis, transwell/migration assay, and Western blotting assay were performed to detect the relation between PCAT7 and malignant behaviors of NSCLC cells in vitro, including cell proliferation, apoptosis, migration, invasion, and epithelial-to-mesenchymal transition (EMT). Rescue assays were carried out to confirm the contribution of PCAT7 to the progression of NSCLC cells by targeting miR-134-5p. RESULTS: PCAT7 was found to be overexpressed in NSCLC tissues (compared with corresponding non-tumor tissues) and NSCLC cells (compared with normal cell line 16-HBE). Overexpression of PCAT7 resulted in the promotion of tumor cell proliferation, inhibition of cells apoptosis, facilitation of cells metastasis, and formation of EMT phenotype, while PCAT7 expression deletion remarkably prohibited cell proliferation, accelerated their apoptosis, weakened metastasis, and reversed EMT to MET. miR-134-5P, as a target gene of PCAT7, restored the effects of down-regulation of PCAT7. CONCLUSIONS: These findings demonstrate that PCAT7 participates in tumor progression in NSCLC by inhibiting miR-134-5p. International Scientific Literature, Inc. 2017-12-24 /pmc/articles/PMC5749158/ /pubmed/29275424 http://dx.doi.org/10.12659/MSM.907904 Text en © Med Sci Monit, 2017 This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Lab/In Vitro Research
Liu, Qiongliang
Wu, Yingying
Xiao, Jie
Zou, Jianyong
Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title_full Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title_fullStr Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title_full_unstemmed Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title_short Long Non-Coding RNA Prostate Cancer-Associated Transcript 7 (PCAT7) Induces Poor Prognosis and Promotes Tumorigenesis by Inhibiting mir-134-5p in Non-Small-Cell Lung (NSCLC)
title_sort long non-coding rna prostate cancer-associated transcript 7 (pcat7) induces poor prognosis and promotes tumorigenesis by inhibiting mir-134-5p in non-small-cell lung (nsclc)
topic Lab/In Vitro Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5749158/
https://www.ncbi.nlm.nih.gov/pubmed/29275424
http://dx.doi.org/10.12659/MSM.907904
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