Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression

Abstract Background Small nucleolar RNA host gene 25 (SNHG25), a long noncoding RNA, has been well-studied in epithelial ovarian cancer. However, the specific functions of SNHG25 in endometrial cancer (EC) have not been studied yet. In this study, we aimed to elucidate the clinical significance of S...

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Autores principales: Yuhua He, Shuifang Xu, Yi Qi, Jinfang Tian, Fengying Xu
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Publicado: BMC 2021
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spelling oai:doaj.org-article:5e66c9b5bdbe46a9a205786e333a7ec22021-11-21T12:32:09ZLong noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression10.1186/s13048-021-00906-w1757-2215https://doaj.org/article/5e66c9b5bdbe46a9a205786e333a7ec22021-11-01T00:00:00Zhttps://doi.org/10.1186/s13048-021-00906-whttps://doaj.org/toc/1757-2215Abstract Background Small nucleolar RNA host gene 25 (SNHG25), a long noncoding RNA, has been well-studied in epithelial ovarian cancer. However, the specific functions of SNHG25 in endometrial cancer (EC) have not been studied yet. In this study, we aimed to elucidate the clinical significance of SNHG25 in EC and determine the regulatory activity of SNHG25 on the tumor-associated EC phenotype. We also thoroughly explored the molecular mechanisms underlying SNHG25 function in EC. Methods Gene expression was measured using quantitative real-time polymerase chain reaction. The detailed functions of SNHG25 in EC were examined by performing loss-of-function experiments. Moreover, the regulatory mechanisms involving SNHG25, microRNA-497-5p, and fatty acid synthase (FASN) were unveiled using the luciferase reporter assay and RNA immunoprecipitation. Results We observed a high level of SNHG25 in EC using the TCGA dataset and our study cohort. Patients with a high SNHG25 level had shorter overall survival than those with a low SNHG25 level. SNHG25 deficiency resulted in tumor-repressing activities in EC cells by decreasing cell proliferation, migration, and invasion and promoting cell apoptosis. Furthermore, the function of SNHG25 depletion in impairing tumor growth in vivo was confirmed. SNHG25 sequestered miR-497-5p as a competing endogenous RNA in EC and consequently positively regulated FASN expression. Thus, the decrease in miR-497-5p or increase in FASN could neutralize the modulatory actions of SNHG25 knockdown in EC cells. Conclusions The depletion of SNHG25 impedes the oncogenicity of EC by targeting the miR-497-5p/FASN axis. The newly elucidated SNHG25/miR-497-5p/FASN pathway may be a promising target for the molecular-targeted management of EC.Yuhua HeShuifang XuYi QiJinfang TianFengying XuBMCarticleSNHG25Endometrial cancerceRNAmiRNA spongeGynecology and obstetricsRG1-991ENJournal of Ovarian Research, Vol 14, Iss 1, Pp 1-13 (2021)
institution DOAJ
collection DOAJ
language EN
topic SNHG25
Endometrial cancer
ceRNA
miRNA sponge
Gynecology and obstetrics
RG1-991
spellingShingle SNHG25
Endometrial cancer
ceRNA
miRNA sponge
Gynecology and obstetrics
RG1-991
Yuhua He
Shuifang Xu
Yi Qi
Jinfang Tian
Fengying Xu
Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
description Abstract Background Small nucleolar RNA host gene 25 (SNHG25), a long noncoding RNA, has been well-studied in epithelial ovarian cancer. However, the specific functions of SNHG25 in endometrial cancer (EC) have not been studied yet. In this study, we aimed to elucidate the clinical significance of SNHG25 in EC and determine the regulatory activity of SNHG25 on the tumor-associated EC phenotype. We also thoroughly explored the molecular mechanisms underlying SNHG25 function in EC. Methods Gene expression was measured using quantitative real-time polymerase chain reaction. The detailed functions of SNHG25 in EC were examined by performing loss-of-function experiments. Moreover, the regulatory mechanisms involving SNHG25, microRNA-497-5p, and fatty acid synthase (FASN) were unveiled using the luciferase reporter assay and RNA immunoprecipitation. Results We observed a high level of SNHG25 in EC using the TCGA dataset and our study cohort. Patients with a high SNHG25 level had shorter overall survival than those with a low SNHG25 level. SNHG25 deficiency resulted in tumor-repressing activities in EC cells by decreasing cell proliferation, migration, and invasion and promoting cell apoptosis. Furthermore, the function of SNHG25 depletion in impairing tumor growth in vivo was confirmed. SNHG25 sequestered miR-497-5p as a competing endogenous RNA in EC and consequently positively regulated FASN expression. Thus, the decrease in miR-497-5p or increase in FASN could neutralize the modulatory actions of SNHG25 knockdown in EC cells. Conclusions The depletion of SNHG25 impedes the oncogenicity of EC by targeting the miR-497-5p/FASN axis. The newly elucidated SNHG25/miR-497-5p/FASN pathway may be a promising target for the molecular-targeted management of EC.
format article
author Yuhua He
Shuifang Xu
Yi Qi
Jinfang Tian
Fengying Xu
author_facet Yuhua He
Shuifang Xu
Yi Qi
Jinfang Tian
Fengying Xu
author_sort Yuhua He
title Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
title_short Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
title_full Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
title_fullStr Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
title_full_unstemmed Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression
title_sort long noncoding rna snhg25 promotes the malignancy of endometrial cancer by sponging microrna-497-5p and increasing fasn expression
publisher BMC
publishDate 2021
url https://doaj.org/article/5e66c9b5bdbe46a9a205786e333a7ec2
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AT shuifangxu longnoncodingrnasnhg25promotesthemalignancyofendometrialcancerbyspongingmicrorna4975pandincreasingfasnexpression
AT yiqi longnoncodingrnasnhg25promotesthemalignancyofendometrialcancerbyspongingmicrorna4975pandincreasingfasnexpression
AT jinfangtian longnoncodingrnasnhg25promotesthemalignancyofendometrialcancerbyspongingmicrorna4975pandincreasingfasnexpression
AT fengyingxu longnoncodingrnasnhg25promotesthemalignancyofendometrialcancerbyspongingmicrorna4975pandincreasingfasnexpression
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