Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway

Long non-coding RNA MEG3 has been identified as a tumor suppressor which plays important roles in tumorigenesis; however, its potential role in breast cancer has not been fully examined. Here, we showed that MEG3 was downregulated in breast cancer tissues and cell lines. Overexpression of MEG3 inhib...

Full description

Saved in:
Bibliographic Details
Main Authors: Chen-yu Zhang, Ming-sheng Yu, Xiang Li, Zhe Zhang, Ce-ran Han, Bo Yan
Format: Article
Language:English
Published: SAGE Publishing 2017-06-01
Series:Tumor Biology
Online Access:https://doi.org/10.1177/1010428317701311
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1849251290057539584
author Chen-yu Zhang
Ming-sheng Yu
Xiang Li
Zhe Zhang
Ce-ran Han
Bo Yan
author_facet Chen-yu Zhang
Ming-sheng Yu
Xiang Li
Zhe Zhang
Ce-ran Han
Bo Yan
author_sort Chen-yu Zhang
collection DOAJ
description Long non-coding RNA MEG3 has been identified as a tumor suppressor which plays important roles in tumorigenesis; however, its potential role in breast cancer has not been fully examined. Here, we showed that MEG3 was downregulated in breast cancer tissues and cell lines. Overexpression of MEG3 inhibited breast cancer cell proliferation and invasion, suggesting that MEG3 played an important role in breast cancer progression and metastasis. Moreover, MEG3 upregulation caused marked inhibition of angiogenesis-related factor expression. Conditioned medium derived from MEG3 overexpressed breast cancer cells significantly decreased the capillary tube formation of endothelial cells. Furthermore, elevated expression of MEG3 in breast cancer inhibits in vivo tumorigenesis and angiogenesis in a nude mouse xenograft model. Mechanistically, overexpression of MEG3 results in downregulation of AKT signaling, which is pivotal for breast cancer cell growth, invasion, and tumor angiogenesis. Collectively, these results suggest that MEG3 might suppress the tumor growth and angiogenesis via AKT signaling pathway and MEG3 may serve as a potential novel diagnostic and therapeutic target of breast cancer.
format Article
id doaj-art-92ebe8e6aea4495dbee978b7b1cade32
institution Kabale University
issn 1423-0380
language English
publishDate 2017-06-01
publisher SAGE Publishing
record_format Article
series Tumor Biology
spelling doaj-art-92ebe8e6aea4495dbee978b7b1cade322025-08-20T03:56:59ZengSAGE PublishingTumor Biology1423-03802017-06-013910.1177/1010428317701311Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathwayChen-yu Zhang0Ming-sheng Yu1Xiang Li2Zhe Zhang3Ce-ran Han4Bo Yan5Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of General Surgery, Shanghai Pudong District People’s Hospital, Shanghai, ChinaDepartment of General Surgery, Shanghai Pudong District People’s Hospital, Shanghai, ChinaLong non-coding RNA MEG3 has been identified as a tumor suppressor which plays important roles in tumorigenesis; however, its potential role in breast cancer has not been fully examined. Here, we showed that MEG3 was downregulated in breast cancer tissues and cell lines. Overexpression of MEG3 inhibited breast cancer cell proliferation and invasion, suggesting that MEG3 played an important role in breast cancer progression and metastasis. Moreover, MEG3 upregulation caused marked inhibition of angiogenesis-related factor expression. Conditioned medium derived from MEG3 overexpressed breast cancer cells significantly decreased the capillary tube formation of endothelial cells. Furthermore, elevated expression of MEG3 in breast cancer inhibits in vivo tumorigenesis and angiogenesis in a nude mouse xenograft model. Mechanistically, overexpression of MEG3 results in downregulation of AKT signaling, which is pivotal for breast cancer cell growth, invasion, and tumor angiogenesis. Collectively, these results suggest that MEG3 might suppress the tumor growth and angiogenesis via AKT signaling pathway and MEG3 may serve as a potential novel diagnostic and therapeutic target of breast cancer.https://doi.org/10.1177/1010428317701311
spellingShingle Chen-yu Zhang
Ming-sheng Yu
Xiang Li
Zhe Zhang
Ce-ran Han
Bo Yan
Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
Tumor Biology
title Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
title_full Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
title_fullStr Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
title_full_unstemmed Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
title_short Overexpression of long non-coding RNA MEG3 suppresses breast cancer cell proliferation, invasion, and angiogenesis through AKT pathway
title_sort overexpression of long non coding rna meg3 suppresses breast cancer cell proliferation invasion and angiogenesis through akt pathway
url https://doi.org/10.1177/1010428317701311
work_keys_str_mv AT chenyuzhang overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway
AT mingshengyu overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway
AT xiangli overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway
AT zhezhang overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway
AT ceranhan overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway
AT boyan overexpressionoflongnoncodingrnameg3suppressesbreastcancercellproliferationinvasionandangiogenesisthroughaktpathway