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The long non-coding RNA HOTAIR increases tumour growth and invasion in cervical cancer by targeting the Notch pathway
DC Field | Value | Language |
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dc.contributor.author | 김상운 | - |
dc.contributor.author | 김영태 | - |
dc.contributor.author | 전경희 | - |
dc.contributor.author | 조남훈 | - |
dc.date.accessioned | 2017-10-26T07:11:21Z | - |
dc.date.available | 2017-10-26T07:11:21Z | - |
dc.date.issued | 2016 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/151713 | - |
dc.description.abstract | Evidence suggests that the long non-coding RNA (lncRNA), HOTAIR, is involved in cervical cancer pathogenesis. We examined serum HOTAIR expression levels in cervical cancer patients and determined the relationships between HOTAIR expression and several clinicopathological factors, including survival. We also examined the functional consequences of HOTAIR overexpression both in vitro and in vivo. Compared with control patients, HOTAIR expression was significantly greater in the serum of cervical cancer patients (P < 0.001). The results indicated that this increase was significantly associated with tumour size (P = 0.030), lymphovascular space invasion (P = 0.037), and lymph node metastasis (P = 0.043). Univariate analysis revealed that disease-free survival and overall survival times were significantly shorter in cervical cancer patients with high HOTAIR expression (hazard ratio [HR] = 4.27, 4.68 and P = 0.039, 0.031, respectively). Cell proliferation and invasion in vitro increased as a result of lentiviral-mediated HOTAIR overexpression in cervical cancer cell lines. HOTAIR knockdown inhibited these properties and increased apoptosis. In vivo xenograft experiments using the HOTAIR-overexpressing SiHa cell line revealed that HOTAIR was a strong inducer of tumour growth and modulated the expression of epithelial-mesenchymal transition and Notch-Wnt signalling pathway-related genes. This result suggested that HOTAIR overexpression promoted cell proliferation and invasion. In conclusion, increased HOTAIR expression was associated with decreased patient survival times. HOTAIR may be a useful target for treatment of cervical cancer patients. | - |
dc.description.statementOfResponsibility | open | - |
dc.format | application/pdf | - |
dc.language | English | - |
dc.publisher | Impact Journals | - |
dc.relation.isPartOf | ONCOTARGET | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Adult | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Cell Line, Tumor | - |
dc.subject.MESH | Female | - |
dc.subject.MESH | Gene Expression Regulation, Neoplastic* | - |
dc.subject.MESH | Humans | - |
dc.subject.MESH | Kaplan-Meier Estimate | - |
dc.subject.MESH | Magnetic Resonance Imaging | - |
dc.subject.MESH | Mice, Inbred BALB C | - |
dc.subject.MESH | Middle Aged | - |
dc.subject.MESH | Neoplasm Invasiveness | - |
dc.subject.MESH | Positron-Emission Tomography | - |
dc.subject.MESH | RNA, Long Noncoding/genetics* | - |
dc.subject.MESH | Receptors, Notch/genetics* | - |
dc.subject.MESH | Signal Transduction/genetics* | - |
dc.subject.MESH | Transplantation, Heterologous | - |
dc.subject.MESH | Tumor Burden/genetics | - |
dc.subject.MESH | Uterine Cervical Neoplasms/diagnostic imaging | - |
dc.subject.MESH | Uterine Cervical Neoplasms/genetics* | - |
dc.subject.MESH | Uterine Cervical Neoplasms/pathology | - |
dc.title | The long non-coding RNA HOTAIR increases tumour growth and invasion in cervical cancer by targeting the Notch pathway | - |
dc.type | Article | - |
dc.publisher.location | United States | - |
dc.contributor.college | College of Medicine | - |
dc.contributor.department | Dept. of Obstetrics & Gynecology | - |
dc.contributor.googleauthor | Maria Lee | - |
dc.contributor.googleauthor | Hee Jung Kim | - |
dc.contributor.googleauthor | Sang Wun Kim | - |
dc.contributor.googleauthor | Sun-Ae Park | - |
dc.contributor.googleauthor | Kyung-Hee Chun | - |
dc.contributor.googleauthor | Nam Hoon Cho | - |
dc.contributor.googleauthor | Yong Sang Song | - |
dc.contributor.googleauthor | Young Tae Kim | - |
dc.identifier.doi | 10.18632/oncotarget.10065 | - |
dc.contributor.localId | A00729 | - |
dc.contributor.localId | A03501 | - |
dc.contributor.localId | A03812 | - |
dc.contributor.localId | A00526 | - |
dc.relation.journalcode | J02421 | - |
dc.identifier.eissn | 1949-2553 | - |
dc.identifier.pmid | 27323817 | - |
dc.subject.keyword | HOTAIR | - |
dc.subject.keyword | cervical cancer | - |
dc.subject.keyword | invasion | - |
dc.subject.keyword | long non-coding RNA | - |
dc.subject.keyword | prognosis | - |
dc.contributor.alternativeName | Kim, Sang Wun | - |
dc.contributor.alternativeName | Kim, Young Tae | - |
dc.contributor.alternativeName | Chun, Kyung Hee | - |
dc.contributor.alternativeName | Cho, Nam Hoon | - |
dc.contributor.affiliatedAuthor | Kim, Young Tae | - |
dc.contributor.affiliatedAuthor | Chun, Kyung Hee | - |
dc.contributor.affiliatedAuthor | Cho, Nam Hoon | - |
dc.contributor.affiliatedAuthor | Kim, Sang Wun | - |
dc.citation.volume | 7 | - |
dc.citation.number | 28 | - |
dc.citation.startPage | 44558 | - |
dc.citation.endPage | 44571 | - |
dc.identifier.bibliographicCitation | ONCOTARGET, Vol.7(28) : 44558-44571, 2016 | - |
dc.date.modified | 2017-10-24 | - |
dc.identifier.rimsid | 45726 | - |
dc.type.rims | ART | - |
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