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MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2

BACKGROUND: MicroRNAs (miRNAs) have emerged as the critical modulators of the tumorigenesis and tumor progression. METHODS: The levels of miR-663 in ovarian cancer cell lines and clinical tissues were detected using qRT-PCR assays. The Transwell invasion and wound healing assay were conducted to ass...

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Autores principales: Xie, Hui Hui, Huan, Wen Ting, Han, Jiang Qiong, Ren, Wei Ru, Yang, Li Hua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448305/
https://www.ncbi.nlm.nih.gov/pubmed/30944041
http://dx.doi.org/10.1186/s40659-019-0219-6
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author Xie, Hui Hui
Huan, Wen Ting
Han, Jiang Qiong
Ren, Wei Ru
Yang, Li Hua
author_facet Xie, Hui Hui
Huan, Wen Ting
Han, Jiang Qiong
Ren, Wei Ru
Yang, Li Hua
author_sort Xie, Hui Hui
collection PubMed
description BACKGROUND: MicroRNAs (miRNAs) have emerged as the critical modulators of the tumorigenesis and tumor progression. METHODS: The levels of miR-663 in ovarian cancer cell lines and clinical tissues were detected using qRT-PCR assays. The Transwell invasion and wound healing assay were conducted to assess the roles of miR-663 in the migration and invasion of ovarian cancer cell in vitro. Rescue assays were carried out to confirm the contribution of tumor suppressor candidate 2 (TUSC2) in the aggressiveness of cancer cell which was regulated by miR-663. RESULTS: The levels of miR-663 were up-regulated in ovarian cancer tissues in comparison with the corresponding normal tissues. Up-regulation of miR-663 increased the proliferation, colony formation, migration and invasion of ovarian cancer SKOV3 cell. Additional, over-expression of miR-663 increased the tumor growth of SKOV3 in xenograft model. Bioinformatics analysis and luciferase reporter assay identified that miR-663 decreased the level of TUSC2 via binding to the 3′-UTR of TUSC2 gene. Finally, the expression of TUSC2 was inversely associated with the level of miR-663 in ovarian carcinoma tissue and over-expression of TUSC2 inhibited the migration and invasion abilities of SKOV3 that was promoted by miR-663. CONCLUSION: Altogether, these results indicate that miR-663 acts as a potential tumor-promoting miRNA through targeting TUSC2 in ovarian cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s40659-019-0219-6) contains supplementary material, which is available to authorized users.
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spelling pubmed-64483052019-04-15 MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2 Xie, Hui Hui Huan, Wen Ting Han, Jiang Qiong Ren, Wei Ru Yang, Li Hua Biol Res Research Article BACKGROUND: MicroRNAs (miRNAs) have emerged as the critical modulators of the tumorigenesis and tumor progression. METHODS: The levels of miR-663 in ovarian cancer cell lines and clinical tissues were detected using qRT-PCR assays. The Transwell invasion and wound healing assay were conducted to assess the roles of miR-663 in the migration and invasion of ovarian cancer cell in vitro. Rescue assays were carried out to confirm the contribution of tumor suppressor candidate 2 (TUSC2) in the aggressiveness of cancer cell which was regulated by miR-663. RESULTS: The levels of miR-663 were up-regulated in ovarian cancer tissues in comparison with the corresponding normal tissues. Up-regulation of miR-663 increased the proliferation, colony formation, migration and invasion of ovarian cancer SKOV3 cell. Additional, over-expression of miR-663 increased the tumor growth of SKOV3 in xenograft model. Bioinformatics analysis and luciferase reporter assay identified that miR-663 decreased the level of TUSC2 via binding to the 3′-UTR of TUSC2 gene. Finally, the expression of TUSC2 was inversely associated with the level of miR-663 in ovarian carcinoma tissue and over-expression of TUSC2 inhibited the migration and invasion abilities of SKOV3 that was promoted by miR-663. CONCLUSION: Altogether, these results indicate that miR-663 acts as a potential tumor-promoting miRNA through targeting TUSC2 in ovarian cancer. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1186/s40659-019-0219-6) contains supplementary material, which is available to authorized users. BioMed Central 2019-04-03 /pmc/articles/PMC6448305/ /pubmed/30944041 http://dx.doi.org/10.1186/s40659-019-0219-6 Text en © The Author(s) 2019 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Xie, Hui Hui
Huan, Wen Ting
Han, Jiang Qiong
Ren, Wei Ru
Yang, Li Hua
MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title_full MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title_fullStr MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title_full_unstemmed MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title_short MicroRNA-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting TUSC2
title_sort microrna-663 facilitates the growth, migration and invasion of ovarian cancer cell by inhibiting tusc2
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6448305/
https://www.ncbi.nlm.nih.gov/pubmed/30944041
http://dx.doi.org/10.1186/s40659-019-0219-6
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