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

HOXA 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...

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Autores principales: Eoh, Kyung Jin, Lee, Dae Woo, Nam, Eun Ji, Kim, Jae In, Moon, Hanna, Kim, Sang Wun, Kim, Young Tae
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9944947/
https://www.ncbi.nlm.nih.gov/pubmed/36799173
http://dx.doi.org/10.3892/or.2023.8501
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author Eoh, Kyung Jin
Lee, Dae Woo
Nam, Eun Ji
Kim, Jae In
Moon, Hanna
Kim, Sang Wun
Kim, Young Tae
author_facet Eoh, Kyung Jin
Lee, Dae Woo
Nam, Eun Ji
Kim, Jae In
Moon, Hanna
Kim, Sang Wun
Kim, Young Tae
author_sort Eoh, Kyung Jin
collection PubMed
description HOXA 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 experiments 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.
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spelling pubmed-99449472023-02-23 HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer Eoh, Kyung Jin Lee, Dae Woo Nam, Eun Ji Kim, Jae In Moon, Hanna Kim, Sang Wun Kim, Young Tae Oncol Rep Articles HOXA 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 experiments 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. D.A. Spandidos 2023-02-14 /pmc/articles/PMC9944947/ /pubmed/36799173 http://dx.doi.org/10.3892/or.2023.8501 Text en Copyright: © Eoh et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Eoh, Kyung Jin
Lee, Dae Woo
Nam, Eun Ji
Kim, Jae In
Moon, Hanna
Kim, Sang Wun
Kim, Young Tae
HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title_full HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title_fullStr HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title_full_unstemmed HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title_short HOXA‑AS3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
title_sort hoxa‑as3 induces tumor progression through the epithelial‑mesenchymal transition pathway in epithelial ovarian cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9944947/
https://www.ncbi.nlm.nih.gov/pubmed/36799173
http://dx.doi.org/10.3892/or.2023.8501
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