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HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer

DC Field Value Language
dc.contributor.author김상운-
dc.contributor.author김영태-
dc.contributor.author남은지-
dc.contributor.author어경진-
dc.date.accessioned2023-04-20T08:24:43Z-
dc.date.available2023-04-20T08:24:43Z-
dc.date.issued2023-03-
dc.identifier.issn1021-335X-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/194083-
dc.description.abstractHOXA cluster antisense RNA 3 (HOXA-AS3) is considered to be involved in several malignancies, however, its biological function in the progression of epithelial ovarian cancer (EOC) remains unclear. The present study compared the expression of HOXA-AS3 in ovarian cancer and normal ovarian tissues and analyzed the association between the expression of HOXA-AS3 and the survival outcomes of patients with ovarian cancer. RNA interference was used to suppress HOXA-AS3 expression in ovarian cancer cell lines in order to demonstrate the function of HOXA-AS3 in ovarian cancer progression. The associations between HOXA-AS3 and epithelial-mesenchymal transition (EMT) markers were explored to verify the mechanism of action of HOXA-AS3 in ovarian cancer. The results of the present study revealed that ovarian cancer tissues exhibited higher HOXA-AS3 expression than normal ovarian tissues. Clinical data indicated that HOXA-AS3 was a significant predictor of progression-free survival and overall survival. Patients with high HOXA-AS3 expression had a poorer prognosis than patients with low HOXA-AS3 expression. In vitro experi- ments using HOXA-AS3-knockdown ovarian cancer cell lines demonstrated that HOXA-AS3 knockdown inhibited cell proliferation and migration. HOXA-AS3 was a potent inducer and modulator of the expression of EMT pathway-related markers and interacted with both the mRNA and protein forms of HOXA3. Collectively, the findings of the present study demonstrated that HOXA-AS3 expression is associated with ovarian cancer progression and thus, may be employed as a prognostic marker and therapeutic target in EOC. © 2023 Spandidos Publications. All rights reserved.-
dc.description.statementOfResponsibilityopen-
dc.languageEnglish-
dc.publisherD.A. Spandidos-
dc.relation.isPartOfONCOLOGY REPORTS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.subject.MESHCarcinoma, Ovarian Epithelial / pathology-
dc.subject.MESHCell Line, Tumor-
dc.subject.MESHCell Movement / genetics-
dc.subject.MESHCell Proliferation / genetics-
dc.subject.MESHEpithelial-Mesenchymal Transition / genetics-
dc.subject.MESHFemale-
dc.subject.MESHGene Expression Regulation, Neoplastic-
dc.subject.MESHHumans-
dc.subject.MESHOvarian Neoplasms* / pathology-
dc.subject.MESHPrognosis-
dc.subject.MESHRNA, Long Noncoding* / genetics-
dc.titleHOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Obstetrics and Gynecology (산부인과학교실)-
dc.contributor.googleauthorKyung Jin Eoh-
dc.contributor.googleauthorDae Woo Lee-
dc.contributor.googleauthorEun Ji Nam-
dc.contributor.googleauthorJae In Kim-
dc.contributor.googleauthorHanna Moon-
dc.contributor.googleauthorSang Wun Kim-
dc.contributor.googleauthorYoung Tae Kim-
dc.identifier.doi10.3892/or.2023.8501-
dc.contributor.localIdA00526-
dc.contributor.localIdA00729-
dc.contributor.localIdA01262-
dc.contributor.localIdA04842-
dc.relation.journalcodeJ02419-
dc.identifier.eissn1791-2431-
dc.identifier.pmid36799173-
dc.subject.keywordHOXA‑AS3-
dc.subject.keywordlong noncoding RNA-
dc.subject.keywordovarian cancer-
dc.subject.keywordprognosis-
dc.subject.keywordprogression-
dc.contributor.alternativeNameKim, Sang Wun-
dc.contributor.affiliatedAuthor김상운-
dc.contributor.affiliatedAuthor김영태-
dc.contributor.affiliatedAuthor남은지-
dc.contributor.affiliatedAuthor어경진-
dc.citation.volume49-
dc.citation.number3-
dc.citation.startPage64-
dc.identifier.bibliographicCitationONCOLOGY REPORTS, Vol.49(3) : 64, 2023-03-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Obstetrics and Gynecology (산부인과학교실) > 1. Journal Papers

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