LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer

Background/Aims: The long noncoding RNA homeobox (HOX) transcript antisense intergenic RNA (HOTAIR) has been demonstrated to be a vital modulator in the proliferation and metastasis of ovarian cancer cells, but its potential molecular mechanism remains to be elucidated. In the current study, we aime...

Full description

Bibliographic Details
Main Authors: Lei  Chang, Ruixia Guo, Zhongfu Yuan, Huirong Shi, Dongya Zhang
Format: Article
Language:English
Published: Cell Physiol Biochem Press GmbH & Co KG 2018-09-01
Series:Cellular Physiology and Biochemistry
Subjects:
Online Access:https://www.karger.com/Article/FullText/493408
id doaj-ea72fac5aeef45d9a1232249a3e17cbf
record_format Article
spelling doaj-ea72fac5aeef45d9a1232249a3e17cbf2020-11-25T00:50:44ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782018-09-014941289130310.1159/000493408493408LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian CancerLei  ChangRuixia GuoZhongfu YuanHuirong ShiDongya ZhangBackground/Aims: The long noncoding RNA homeobox (HOX) transcript antisense intergenic RNA (HOTAIR) has been demonstrated to be a vital modulator in the proliferation and metastasis of ovarian cancer cells, but its potential molecular mechanism remains to be elucidated. In the current study, we aimed to uncover the biological role of lncRNA HOTAIR and its underlying regulatory mechanism in the progression and metastasis of ovarian cancer. Methods: HOTAIR expression was detected by quantitative RT-PCR (qRT-PCR) and northern blotting. The SKOV3 ovarian cancer cell line was chosen for the subsequent assays. In addition, the molecular mRNA and protein expression levels were examined by qRT-PCR and western blotting. The competitive endogenous RNA (ceRNA) mechanism was validated by bioinformatics analysis and a dual luciferase reporter gene assay. Results: HOTAIR expression was significantly higher in ovarian carcinoma tissues and cell lines than in the control counterparts. Both CCND1 and CCND2 were downstream targets of miR-206. The inhibition of HOTAIR elevated the expression of miR-206 and inhibited the expression of CCND1 and CCND2. Moreover, CCND1 and CCND2 were highly expressed in ovarian cancer tissues, and their expression was positively correlated with HOTAIR expression. Finally, the functional assays indicated that the anticancer effects of miR-206 could be rescued by the simultaneous overexpression of either CCND1 or CCND2 in ovarian cancer. Conclusion: HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.https://www.karger.com/Article/FullText/493408LncRNA HOTAIRmiR-206CCND1CCND2Ovarian cancer
collection DOAJ
language English
format Article
sources DOAJ
author Lei  Chang
Ruixia Guo
Zhongfu Yuan
Huirong Shi
Dongya Zhang
spellingShingle Lei  Chang
Ruixia Guo
Zhongfu Yuan
Huirong Shi
Dongya Zhang
LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
Cellular Physiology and Biochemistry
LncRNA HOTAIR
miR-206
CCND1
CCND2
Ovarian cancer
author_facet Lei  Chang
Ruixia Guo
Zhongfu Yuan
Huirong Shi
Dongya Zhang
author_sort Lei  Chang
title LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
title_short LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
title_full LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
title_fullStr LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
title_full_unstemmed LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer
title_sort lncrna hotair regulates ccnd1 and ccnd2 expression by sponging mir-206 in ovarian cancer
publisher Cell Physiol Biochem Press GmbH & Co KG
series Cellular Physiology and Biochemistry
issn 1015-8987
1421-9778
publishDate 2018-09-01
description Background/Aims: The long noncoding RNA homeobox (HOX) transcript antisense intergenic RNA (HOTAIR) has been demonstrated to be a vital modulator in the proliferation and metastasis of ovarian cancer cells, but its potential molecular mechanism remains to be elucidated. In the current study, we aimed to uncover the biological role of lncRNA HOTAIR and its underlying regulatory mechanism in the progression and metastasis of ovarian cancer. Methods: HOTAIR expression was detected by quantitative RT-PCR (qRT-PCR) and northern blotting. The SKOV3 ovarian cancer cell line was chosen for the subsequent assays. In addition, the molecular mRNA and protein expression levels were examined by qRT-PCR and western blotting. The competitive endogenous RNA (ceRNA) mechanism was validated by bioinformatics analysis and a dual luciferase reporter gene assay. Results: HOTAIR expression was significantly higher in ovarian carcinoma tissues and cell lines than in the control counterparts. Both CCND1 and CCND2 were downstream targets of miR-206. The inhibition of HOTAIR elevated the expression of miR-206 and inhibited the expression of CCND1 and CCND2. Moreover, CCND1 and CCND2 were highly expressed in ovarian cancer tissues, and their expression was positively correlated with HOTAIR expression. Finally, the functional assays indicated that the anticancer effects of miR-206 could be rescued by the simultaneous overexpression of either CCND1 or CCND2 in ovarian cancer. Conclusion: HOTAIR enhanced CCND1 and CCND2 expression by negatively modulating miR-206 expression and stimulating the proliferation, cell cycle progression, migration and invasion of ovarian cancer cells.
topic LncRNA HOTAIR
miR-206
CCND1
CCND2
Ovarian cancer
url https://www.karger.com/Article/FullText/493408
work_keys_str_mv AT leichang lncrnahotairregulatesccnd1andccnd2expressionbyspongingmir206inovariancancer
AT ruixiaguo lncrnahotairregulatesccnd1andccnd2expressionbyspongingmir206inovariancancer
AT zhongfuyuan lncrnahotairregulatesccnd1andccnd2expressionbyspongingmir206inovariancancer
AT huirongshi lncrnahotairregulatesccnd1andccnd2expressionbyspongingmir206inovariancancer
AT dongyazhang lncrnahotairregulatesccnd1andccnd2expressionbyspongingmir206inovariancancer
_version_ 1725246827673944064