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hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2

Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_000...

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Autores principales: Zhang, Bowei, Li, Qiaoling, Song, Zhe, Ren, Li, Gu, Yi, Feng, Chao, Wang, Jinju, Liu, Tong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279989/
https://www.ncbi.nlm.nih.gov/pubmed/35447001
http://dx.doi.org/10.1002/jcla.24421
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author Zhang, Bowei
Li, Qiaoling
Song, Zhe
Ren, Li
Gu, Yi
Feng, Chao
Wang, Jinju
Liu, Tong
author_facet Zhang, Bowei
Li, Qiaoling
Song, Zhe
Ren, Li
Gu, Yi
Feng, Chao
Wang, Jinju
Liu, Tong
author_sort Zhang, Bowei
collection PubMed
description Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_0000285) and investigate its modulatory mechanism in THCA progression. We identified the expression profile of hsa_circ_0000285 in THCA by conducting qRT‐PCR assay. Therewith, the potential of hsa_circ_0000285 in THCA development was determined with a set of functional experiments, including CCK‐8, wound healing assay, Western blot, and xenograft model. The molecular mechanism underlying hsa_circ_0000285 was investigated with bioinformatic analysis, RIP and dual‐luciferase reporter experiments. As opposed to normal samples and cells, hsa_circ_0000285 level was overtly increased in THCA specimens and cells. The downregulation of hsa_circ_0000285 weakened the proliferative and migratory capacity of THCA cells and promoted cell apoptosis. In addition, hsa_circ_0000285 silence suppressed the tumor growth of xenograft model mice in vivo. Notably, we demonstrated that hsa_circ_0000285 might target miR‐127‐5p/CDH2 axis in THCA. Afterward, our findings manifested that miR‐127‐5p attenuation blocked the function of hsa_circ_0000285 depletion in THCA cells. In the final step, CDH2 was proven to mediate the repressive potency of miR‐127‐5p in the malignant behaviors of THCA. Mechanistically, hsa_circ_0000285 induced the development of THCA via functioning as a competing endogenous RNA (ceRNA) of miR‐127‐5p to enhance CDH2 expression, which provided a new perspective for THCA therapy.
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spelling pubmed-92799892022-07-15 hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2 Zhang, Bowei Li, Qiaoling Song, Zhe Ren, Li Gu, Yi Feng, Chao Wang, Jinju Liu, Tong J Clin Lab Anal Research Articles Thyroid cancer (THCA) is a leading endocrine cancer and becomes the fifth most commonly diagnosed malignancy in females. It is confirmed that circular RNAs (circRNAs) perform regulatory potencies in the pathological progress of THCA. Our purpose was to certify the trait of hsa_circ_0000285 (circ_0000285) and investigate its modulatory mechanism in THCA progression. We identified the expression profile of hsa_circ_0000285 in THCA by conducting qRT‐PCR assay. Therewith, the potential of hsa_circ_0000285 in THCA development was determined with a set of functional experiments, including CCK‐8, wound healing assay, Western blot, and xenograft model. The molecular mechanism underlying hsa_circ_0000285 was investigated with bioinformatic analysis, RIP and dual‐luciferase reporter experiments. As opposed to normal samples and cells, hsa_circ_0000285 level was overtly increased in THCA specimens and cells. The downregulation of hsa_circ_0000285 weakened the proliferative and migratory capacity of THCA cells and promoted cell apoptosis. In addition, hsa_circ_0000285 silence suppressed the tumor growth of xenograft model mice in vivo. Notably, we demonstrated that hsa_circ_0000285 might target miR‐127‐5p/CDH2 axis in THCA. Afterward, our findings manifested that miR‐127‐5p attenuation blocked the function of hsa_circ_0000285 depletion in THCA cells. In the final step, CDH2 was proven to mediate the repressive potency of miR‐127‐5p in the malignant behaviors of THCA. Mechanistically, hsa_circ_0000285 induced the development of THCA via functioning as a competing endogenous RNA (ceRNA) of miR‐127‐5p to enhance CDH2 expression, which provided a new perspective for THCA therapy. John Wiley and Sons Inc. 2022-04-21 /pmc/articles/PMC9279989/ /pubmed/35447001 http://dx.doi.org/10.1002/jcla.24421 Text en © 2022 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, 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 Research Articles
Zhang, Bowei
Li, Qiaoling
Song, Zhe
Ren, Li
Gu, Yi
Feng, Chao
Wang, Jinju
Liu, Tong
hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title_full hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title_fullStr hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title_full_unstemmed hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title_short hsa_circ_0000285 facilitates thyroid cancer progression by regulating miR‐127‐5p/CDH2
title_sort hsa_circ_0000285 facilitates thyroid cancer progression by regulating mir‐127‐5p/cdh2
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279989/
https://www.ncbi.nlm.nih.gov/pubmed/35447001
http://dx.doi.org/10.1002/jcla.24421
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