MiR-27a Facilitates Breast Cancer Progression via GSK-3β
Breast cancer remains one of the leading causes of cancer-associated death in women. MiR-27a is highly expressed in breast cancer tissue. However, the underlying mechanisms that promote breast cancer progression are unknown. In this study, we investigated the regulatory mechanisms of miR-27a and its...
Main Authors: | , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
SAGE Publishing
2020-10-01
|
Series: | Technology in Cancer Research & Treatment |
Online Access: | https://doi.org/10.1177/1533033820965576 |
_version_ | 1818436751213985792 |
---|---|
author | Huijin Chen BA Yuanyuan Zhang BA Xin Cao BA Peipei Mou BA |
author_facet | Huijin Chen BA Yuanyuan Zhang BA Xin Cao BA Peipei Mou BA |
author_sort | Huijin Chen BA |
collection | DOAJ |
description | Breast cancer remains one of the leading causes of cancer-associated death in women. MiR-27a is highly expressed in breast cancer tissue. However, the underlying mechanisms that promote breast cancer progression are unknown. In this study, we investigated the regulatory mechanisms of miR-27a and its target glycogen Synthase Kinase 3-β (GSK-3β) in breast cancer cells. We found that miR-27a was highly expressed in breast cancer tissues, which downregulated GSK-3β expression. We further identified GSK-3β as a direct target of miR-27a, and found that the miR-27a mediated suppression of GSK-3β activated Wnt/β-catenin-associated proliferative and invasive factor in breast cancer. The cell transfection assay demonstrated the overexpression of miR-27a also enhanced cell proliferation and invasion, and reduced cell apoptosis through GSK-3β. Finally, we demonstrated that the overexpression of miR-27a facilitated breast cancer progression through its ability to down-regulate the phosphorylation of GSK-3β both in vivo and vitro . These findings highlighted miR-27a as a novel therapeutic target in breast cancer. |
first_indexed | 2024-12-14T17:13:45Z |
format | Article |
id | doaj.art-21c9c35a699843adb993d064cf98a3c3 |
institution | Directory Open Access Journal |
issn | 1533-0338 |
language | English |
last_indexed | 2024-12-14T17:13:45Z |
publishDate | 2020-10-01 |
publisher | SAGE Publishing |
record_format | Article |
series | Technology in Cancer Research & Treatment |
spelling | doaj.art-21c9c35a699843adb993d064cf98a3c32022-12-21T22:53:28ZengSAGE PublishingTechnology in Cancer Research & Treatment1533-03382020-10-011910.1177/1533033820965576MiR-27a Facilitates Breast Cancer Progression via GSK-3βHuijin Chen BA0Yuanyuan Zhang BA1Xin Cao BA2Peipei Mou BA3 Department of Clinical Laboratory, ShengLi Oilfield Central Hospital, Dongying, Shandong, China Department of Clinical Laboratory, ShengLi Oilfield Central Hospital, Dongying, Shandong, China Department of Orthopedic Trauma, ShengLi Oilfield Central Hospital, Dongying, Shandong, China Department of Clinical Laboratory, ShengLi Oilfield Central Hospital, Dongying, Shandong, ChinaBreast cancer remains one of the leading causes of cancer-associated death in women. MiR-27a is highly expressed in breast cancer tissue. However, the underlying mechanisms that promote breast cancer progression are unknown. In this study, we investigated the regulatory mechanisms of miR-27a and its target glycogen Synthase Kinase 3-β (GSK-3β) in breast cancer cells. We found that miR-27a was highly expressed in breast cancer tissues, which downregulated GSK-3β expression. We further identified GSK-3β as a direct target of miR-27a, and found that the miR-27a mediated suppression of GSK-3β activated Wnt/β-catenin-associated proliferative and invasive factor in breast cancer. The cell transfection assay demonstrated the overexpression of miR-27a also enhanced cell proliferation and invasion, and reduced cell apoptosis through GSK-3β. Finally, we demonstrated that the overexpression of miR-27a facilitated breast cancer progression through its ability to down-regulate the phosphorylation of GSK-3β both in vivo and vitro . These findings highlighted miR-27a as a novel therapeutic target in breast cancer.https://doi.org/10.1177/1533033820965576 |
spellingShingle | Huijin Chen BA Yuanyuan Zhang BA Xin Cao BA Peipei Mou BA MiR-27a Facilitates Breast Cancer Progression via GSK-3β Technology in Cancer Research & Treatment |
title | MiR-27a Facilitates Breast Cancer Progression via GSK-3β |
title_full | MiR-27a Facilitates Breast Cancer Progression via GSK-3β |
title_fullStr | MiR-27a Facilitates Breast Cancer Progression via GSK-3β |
title_full_unstemmed | MiR-27a Facilitates Breast Cancer Progression via GSK-3β |
title_short | MiR-27a Facilitates Breast Cancer Progression via GSK-3β |
title_sort | mir 27a facilitates breast cancer progression via gsk 3β |
url | https://doi.org/10.1177/1533033820965576 |
work_keys_str_mv | AT huijinchenba mir27afacilitatesbreastcancerprogressionviagsk3b AT yuanyuanzhangba mir27afacilitatesbreastcancerprogressionviagsk3b AT xincaoba mir27afacilitatesbreastcancerprogressionviagsk3b AT peipeimouba mir27afacilitatesbreastcancerprogressionviagsk3b |