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LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer.
Cell Physiol Biochem. 2018; 49(4):1289-1303.CP

Abstract

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.

Authors

No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30205383

Citation

Chang, Lei, et al. "LncRNA HOTAIR Regulates CCND1 and CCND2 Expression By Sponging miR-206 in Ovarian Cancer." Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, vol. 49, no. 4, 2018, pp. 1289-1303.
Chang L, Guo R, Yuan Z, et al. LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer. Cell Physiol Biochem. 2018;49(4):1289-1303.
Chang, L., Guo, R., Yuan, Z., Shi, H., & Zhang, D. (2018). LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer. Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology, 49(4), 1289-1303. https://doi.org/10.1159/000493408
Chang L, et al. LncRNA HOTAIR Regulates CCND1 and CCND2 Expression By Sponging miR-206 in Ovarian Cancer. Cell Physiol Biochem. 2018;49(4):1289-1303. PubMed PMID: 30205383.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - LncRNA HOTAIR Regulates CCND1 and CCND2 Expression by Sponging miR-206 in Ovarian Cancer. AU - Chang,Lei, AU - Guo,Ruixia, AU - Yuan,Zhongfu, AU - Shi,Huirong, AU - Zhang,Dongya, Y1 - 2018/09/11/ PY - 2017/09/25/received PY - 2018/09/03/accepted PY - 2018/9/12/pubmed PY - 2018/10/17/medline PY - 2018/9/12/entrez KW - CCND1 KW - CCND2 KW - LncRNA HOTAIR KW - Ovarian cancer KW - miR-206 SP - 1289 EP - 1303 JF - Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology JO - Cell. Physiol. Biochem. VL - 49 IS - 4 N2 - 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. SN - 1421-9778 UR - https://www.unboundmedicine.com/medline/citation/30205383/LncRNA_HOTAIR_Regulates_CCND1_and_CCND2_Expression_by_Sponging_miR_206_in_Ovarian_Cancer_ L2 - https://www.karger.com?DOI=10.1159/000493408 DB - PRIME DP - Unbound Medicine ER -