MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2

A large number of studies have shown that microRNA (miRNA) has an important relationship with the occurrence and development of colorectal cancer (CRC), but its specific molecular mechanism has not been fully elucidated. This study is to explore the influence of miR-506-3p on the malignant behavior...

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Main Authors: Liang Ai, Xiaojun Luo, Xiong Yan, Shan Jiang
Format: Article
Language:English
Published: Taylor & Francis Group 2021-01-01
Series:Bioengineered
Subjects:
Online Access:http://dx.doi.org/10.1080/21655979.2021.1951930
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spelling doaj-37f862c1fe0640f893d4295a421f5b172021-09-06T14:06:26ZengTaylor & Francis GroupBioengineered2165-59792165-59872021-01-011214044405310.1080/21655979.2021.19519301951930MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2Liang Ai0Xiaojun Luo1Xiong Yan2Shan Jiang3Chongqing Hospital of Traditional Chinese MedicineChongqing University Cancer HospitalThe First Affiliated Hospital of Chongqing Medical UniversityThe First Affiliated Hospital of Chongqing Medical UniversityA large number of studies have shown that microRNA (miRNA) has an important relationship with the occurrence and development of colorectal cancer (CRC), but its specific molecular mechanism has not been fully elucidated. This study is to explore the influence of miR-506-3p on the malignant behavior of CRC and its underlying molecular mechanism. Our results show that miR-506-3p was lowly expressed and enhancer of zeste homologue 2 (EZH2) was highly expressed in CRC. Overexpressing miR-506-3p or silencing EZH2 inhibited CRC cell proliferation, migration and invasion and promoted apoptosis. Inhibiting miR-506-3p promoted CRC cell proliferation, migration and invasion but inhibited apoptosis. These impacts were reversed after co-transfecting si-EZH2. Further mechanism studies have shown that miR-506-3p can reduce EZH2 expression in CRC cells by binding to the 3ʹUTR end of EZH2. In summary, the results of this study show that miR-506-3p inhibited CRC progression through targeting EZH2 expression. This provides a new molecular target for the clinical treatment of CRC in the future.http://dx.doi.org/10.1080/21655979.2021.1951930mir-506-3pcolorectal cancerenhancer of zeste homologue 2 (ezh2)
collection DOAJ
language English
format Article
sources DOAJ
author Liang Ai
Xiaojun Luo
Xiong Yan
Shan Jiang
spellingShingle Liang Ai
Xiaojun Luo
Xiong Yan
Shan Jiang
MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
Bioengineered
mir-506-3p
colorectal cancer
enhancer of zeste homologue 2 (ezh2)
author_facet Liang Ai
Xiaojun Luo
Xiong Yan
Shan Jiang
author_sort Liang Ai
title MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
title_short MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
title_full MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
title_fullStr MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
title_full_unstemmed MicroRNA-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
title_sort microrna-506-3p inhibits colorectal cancer cell proliferation through targeting enhancer of zeste homologue 2
publisher Taylor & Francis Group
series Bioengineered
issn 2165-5979
2165-5987
publishDate 2021-01-01
description A large number of studies have shown that microRNA (miRNA) has an important relationship with the occurrence and development of colorectal cancer (CRC), but its specific molecular mechanism has not been fully elucidated. This study is to explore the influence of miR-506-3p on the malignant behavior of CRC and its underlying molecular mechanism. Our results show that miR-506-3p was lowly expressed and enhancer of zeste homologue 2 (EZH2) was highly expressed in CRC. Overexpressing miR-506-3p or silencing EZH2 inhibited CRC cell proliferation, migration and invasion and promoted apoptosis. Inhibiting miR-506-3p promoted CRC cell proliferation, migration and invasion but inhibited apoptosis. These impacts were reversed after co-transfecting si-EZH2. Further mechanism studies have shown that miR-506-3p can reduce EZH2 expression in CRC cells by binding to the 3ʹUTR end of EZH2. In summary, the results of this study show that miR-506-3p inhibited CRC progression through targeting EZH2 expression. This provides a new molecular target for the clinical treatment of CRC in the future.
topic mir-506-3p
colorectal cancer
enhancer of zeste homologue 2 (ezh2)
url http://dx.doi.org/10.1080/21655979.2021.1951930
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AT xiaojunluo microrna5063pinhibitscolorectalcancercellproliferationthroughtargetingenhancerofzestehomologue2
AT xiongyan microrna5063pinhibitscolorectalcancercellproliferationthroughtargetingenhancerofzestehomologue2
AT shanjiang microrna5063pinhibitscolorectalcancercellproliferationthroughtargetingenhancerofzestehomologue2
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