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Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade

BACKGROUND: Circular RNAs (circRNAs) play important roles in various malignancies, such as colorectal cancer (CRC). However, the function of hsa_circ_0001550 in CRC remains to be elucidated. METHODS: The expression levels of hsa_circ_0001550, microRNA (miR)‐4262, and nuclear casein kinase and cyclin...

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Autores principales: Zhou, Ying, Zhang, Qilin, Qiu, Xiaofeng, Tian, Tianning, Xu, Qihua, Liao, Bingling
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/PMC9279960/
https://www.ncbi.nlm.nih.gov/pubmed/35698305
http://dx.doi.org/10.1002/jcla.24532
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author Zhou, Ying
Zhang, Qilin
Qiu, Xiaofeng
Tian, Tianning
Xu, Qihua
Liao, Bingling
author_facet Zhou, Ying
Zhang, Qilin
Qiu, Xiaofeng
Tian, Tianning
Xu, Qihua
Liao, Bingling
author_sort Zhou, Ying
collection PubMed
description BACKGROUND: Circular RNAs (circRNAs) play important roles in various malignancies, such as colorectal cancer (CRC). However, the function of hsa_circ_0001550 in CRC remains to be elucidated. METHODS: The expression levels of hsa_circ_0001550, microRNA (miR)‐4262, and nuclear casein kinase and cyclin‐dependent kinase substrate 1 (NUCKS1) were determined by real‐time qPCR. Cell biological behaviors were evaluated via colony formation assay, transwell assay, flow cytometry, and sphere formation assays. The target relationship was validated via dual‐luciferase reporter and RNA pull‐down assays. Protein expression was analyzed by western blot. Xenograft tumor model was adopted to evaluate hsa_circ_0001550 function in vivo. RESULTS: Hsa_circ_0001550 enrichment was enhanced in CRC tissue specimens and cell lines. Hsa_circ_0001550 absence hindered CRC cell proliferation, metastasis, stemness, and caused apoptosis. Hsa_circ_0001550 targeted miR‐4262, and hsa_circ_0001550 absence‐caused impacts were diminished by anti‐miR‐4262. MiR‐4262 targeted NUCKS1. Hsa_circ_0001550 had positive regulation on NUCKS1 expression. NUCKS1 overexpression overturned the influences of hsa_circ_0001550 silencingon CRC cell progression. Hsa_circ_0001550 interference notably blocked in vivo xenograft tumor growth. CONCLUSION: Hsa_circ_0001550 facilitated CRC progression by binding to miR‐4262 to positively regulate NUCKS1 abundance.
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spelling pubmed-92799602022-07-15 Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade Zhou, Ying Zhang, Qilin Qiu, Xiaofeng Tian, Tianning Xu, Qihua Liao, Bingling J Clin Lab Anal Research Articles BACKGROUND: Circular RNAs (circRNAs) play important roles in various malignancies, such as colorectal cancer (CRC). However, the function of hsa_circ_0001550 in CRC remains to be elucidated. METHODS: The expression levels of hsa_circ_0001550, microRNA (miR)‐4262, and nuclear casein kinase and cyclin‐dependent kinase substrate 1 (NUCKS1) were determined by real‐time qPCR. Cell biological behaviors were evaluated via colony formation assay, transwell assay, flow cytometry, and sphere formation assays. The target relationship was validated via dual‐luciferase reporter and RNA pull‐down assays. Protein expression was analyzed by western blot. Xenograft tumor model was adopted to evaluate hsa_circ_0001550 function in vivo. RESULTS: Hsa_circ_0001550 enrichment was enhanced in CRC tissue specimens and cell lines. Hsa_circ_0001550 absence hindered CRC cell proliferation, metastasis, stemness, and caused apoptosis. Hsa_circ_0001550 targeted miR‐4262, and hsa_circ_0001550 absence‐caused impacts were diminished by anti‐miR‐4262. MiR‐4262 targeted NUCKS1. Hsa_circ_0001550 had positive regulation on NUCKS1 expression. NUCKS1 overexpression overturned the influences of hsa_circ_0001550 silencingon CRC cell progression. Hsa_circ_0001550 interference notably blocked in vivo xenograft tumor growth. CONCLUSION: Hsa_circ_0001550 facilitated CRC progression by binding to miR‐4262 to positively regulate NUCKS1 abundance. John Wiley and Sons Inc. 2022-06-13 /pmc/articles/PMC9279960/ /pubmed/35698305 http://dx.doi.org/10.1002/jcla.24532 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
Zhou, Ying
Zhang, Qilin
Qiu, Xiaofeng
Tian, Tianning
Xu, Qihua
Liao, Bingling
Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title_full Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title_fullStr Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title_full_unstemmed Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title_short Hsa_circ_0001550 facilitates colorectal cancer progression through mediating microRNA‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
title_sort hsa_circ_0001550 facilitates colorectal cancer progression through mediating microrna‐4262/nuclear casein kinase and cyclin‐dependent kinase substrate 1 cascade
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9279960/
https://www.ncbi.nlm.nih.gov/pubmed/35698305
http://dx.doi.org/10.1002/jcla.24532
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