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LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p

BACKGROUND: Cervical cancer (CC) is the one of most common malignant gynecological tumors, which is characterized with the high mortality and recurrence rate. Previous studies have elucidated the oncogenic role of small nucleolar RNA host gene 6 (SNHG6) in some types of human cancers, whereas it is...

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Autores principales: Liu, Jin, Liu, Xiaojiao, Li, Rong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457785/
https://www.ncbi.nlm.nih.gov/pubmed/32884447
http://dx.doi.org/10.1186/s12935-020-01448-9
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author Liu, Jin
Liu, Xiaojiao
Li, Rong
author_facet Liu, Jin
Liu, Xiaojiao
Li, Rong
author_sort Liu, Jin
collection PubMed
description BACKGROUND: Cervical cancer (CC) is the one of most common malignant gynecological tumors, which is characterized with the high mortality and recurrence rate. Previous studies have elucidated the oncogenic role of small nucleolar RNA host gene 6 (SNHG6) in some types of human cancers, whereas it is unclear whether it functions as an oncogene in CC. This study was aimed at unveiling the role of SNHG6 in CC. METHODS: qRT-PCR analysis was implemented to evaluate the expression levels of SNHG6, miR-485-3p and STYX in CC cells. RNA pull down assay and luciferase reporter assay were conducted to verify the interaction between miR-485-3p and SNHG6 or STYX. Functional assays, such as colony formation assay, JC-1 assay and TUNEL assay were applied to detect the biological behaviors of CC cells. The resistance of CC cells to radiation was evaluated by colony formation assay. RESULTS: SNHG6 was expressed at a high level in CC cells. Silenced SNHG6 suppressed cell proliferation but promoted cell apoptosis. Additionally, silenced SNHG6 could sensitize CC cells to radiation treatment. miR-485-3p could bind to both SNHG6 and STYX. Knockdown of miR-485-3p or overexpression of STYX could abolish the effects of SNHG6 silencing on CC cell growth. CONCLUSIONS: LncRNA SNHG6 enhances the radioresistance of CC cells and promotes CC cell growth by sponging miR-485-3p to release STYX.
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spelling pubmed-74577852020-09-02 LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p Liu, Jin Liu, Xiaojiao Li, Rong Cancer Cell Int Primary Research BACKGROUND: Cervical cancer (CC) is the one of most common malignant gynecological tumors, which is characterized with the high mortality and recurrence rate. Previous studies have elucidated the oncogenic role of small nucleolar RNA host gene 6 (SNHG6) in some types of human cancers, whereas it is unclear whether it functions as an oncogene in CC. This study was aimed at unveiling the role of SNHG6 in CC. METHODS: qRT-PCR analysis was implemented to evaluate the expression levels of SNHG6, miR-485-3p and STYX in CC cells. RNA pull down assay and luciferase reporter assay were conducted to verify the interaction between miR-485-3p and SNHG6 or STYX. Functional assays, such as colony formation assay, JC-1 assay and TUNEL assay were applied to detect the biological behaviors of CC cells. The resistance of CC cells to radiation was evaluated by colony formation assay. RESULTS: SNHG6 was expressed at a high level in CC cells. Silenced SNHG6 suppressed cell proliferation but promoted cell apoptosis. Additionally, silenced SNHG6 could sensitize CC cells to radiation treatment. miR-485-3p could bind to both SNHG6 and STYX. Knockdown of miR-485-3p or overexpression of STYX could abolish the effects of SNHG6 silencing on CC cell growth. CONCLUSIONS: LncRNA SNHG6 enhances the radioresistance of CC cells and promotes CC cell growth by sponging miR-485-3p to release STYX. BioMed Central 2020-08-31 /pmc/articles/PMC7457785/ /pubmed/32884447 http://dx.doi.org/10.1186/s12935-020-01448-9 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.
spellingShingle Primary Research
Liu, Jin
Liu, Xiaojiao
Li, Rong
LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title_full LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title_fullStr LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title_full_unstemmed LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title_short LncRNA SNHG6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging miR-485-3p
title_sort lncrna snhg6 enhances the radioresistance and promotes the growth of cervical cancer cells by sponging mir-485-3p
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457785/
https://www.ncbi.nlm.nih.gov/pubmed/32884447
http://dx.doi.org/10.1186/s12935-020-01448-9
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