Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway

Abstract Triple-negative breast cancer (TNBC) is a pathological subtype of breast cancer (BC) with high malignancy, strong invasiveness and poor prognosis. Long non-coding RNA (LncRNA) plays an important role during tumorigenesis. We identified that Linc00707 was upregulated in TNBC tissues by TCGA...

Full description

Bibliographic Details
Main Authors: Hongli Li, Qinghua Liu, Yaqiong Hu, Chonggao Yin, Yunxiang Zhang, Peng Gao
Format: Article
Language:English
Published: Nature Publishing Group 2024-03-01
Series:Cell Death Discovery
Online Access:https://doi.org/10.1038/s41420-024-01906-7
_version_ 1797259542196649984
author Hongli Li
Qinghua Liu
Yaqiong Hu
Chonggao Yin
Yunxiang Zhang
Peng Gao
author_facet Hongli Li
Qinghua Liu
Yaqiong Hu
Chonggao Yin
Yunxiang Zhang
Peng Gao
author_sort Hongli Li
collection DOAJ
description Abstract Triple-negative breast cancer (TNBC) is a pathological subtype of breast cancer (BC) with high malignancy, strong invasiveness and poor prognosis. Long non-coding RNA (LncRNA) plays an important role during tumorigenesis. We identified that Linc00707 was upregulated in TNBC tissues by TCGA database and RT-qPCR assay, compared with normal breast tissues and other subtypes of BC. Linc00707 promoted TNBC cells proliferation, migration and invasion. Furthermore, we found that knockdown of Linc00707 influenced autophagy via PI3K/AKT/mTOR signaling pathway in TNBC cells. Linc00707 affected the progress of TNBC cells through affecting autophagy. Further mechanistic experiments confirmed that Linc00707 could competitively bind with miR-423-5p to up-regulate MARCH2 expression, ultimately promoting TNBC progression and autophagy through PI3K/AKT/mTOR pathway. In conclusion, we demonstrate that Linc00707 is a key molecule in tumor progression and may be an effective target for patients with TNBC.
first_indexed 2024-04-24T23:11:05Z
format Article
id doaj.art-ffc3449ffd1348d697f297c8aff4deff
institution Directory Open Access Journal
issn 2058-7716
language English
last_indexed 2024-04-24T23:11:05Z
publishDate 2024-03-01
publisher Nature Publishing Group
record_format Article
series Cell Death Discovery
spelling doaj.art-ffc3449ffd1348d697f297c8aff4deff2024-03-17T12:14:41ZengNature Publishing GroupCell Death Discovery2058-77162024-03-0110111410.1038/s41420-024-01906-7Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathwayHongli Li0Qinghua Liu1Yaqiong Hu2Chonggao Yin3Yunxiang Zhang4Peng Gao5Department of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong UniversityMedicine Research Center, Shandong Second Medical UniversityMedicine Research Center, Shandong Second Medical UniversityCollege of Nursing, Shandong Second Medical UniversityDepartment of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong UniversityDepartment of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong UniversityAbstract Triple-negative breast cancer (TNBC) is a pathological subtype of breast cancer (BC) with high malignancy, strong invasiveness and poor prognosis. Long non-coding RNA (LncRNA) plays an important role during tumorigenesis. We identified that Linc00707 was upregulated in TNBC tissues by TCGA database and RT-qPCR assay, compared with normal breast tissues and other subtypes of BC. Linc00707 promoted TNBC cells proliferation, migration and invasion. Furthermore, we found that knockdown of Linc00707 influenced autophagy via PI3K/AKT/mTOR signaling pathway in TNBC cells. Linc00707 affected the progress of TNBC cells through affecting autophagy. Further mechanistic experiments confirmed that Linc00707 could competitively bind with miR-423-5p to up-regulate MARCH2 expression, ultimately promoting TNBC progression and autophagy through PI3K/AKT/mTOR pathway. In conclusion, we demonstrate that Linc00707 is a key molecule in tumor progression and may be an effective target for patients with TNBC.https://doi.org/10.1038/s41420-024-01906-7
spellingShingle Hongli Li
Qinghua Liu
Yaqiong Hu
Chonggao Yin
Yunxiang Zhang
Peng Gao
Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
Cell Death Discovery
title Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
title_full Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
title_fullStr Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
title_full_unstemmed Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
title_short Linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of PI3K/AKT/mTOR pathway
title_sort linc00707 regulates autophagy and promotes the progression of triple negative breast cancer by activation of pi3k akt mtor pathway
url https://doi.org/10.1038/s41420-024-01906-7
work_keys_str_mv AT honglili linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway
AT qinghualiu linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway
AT yaqionghu linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway
AT chonggaoyin linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway
AT yunxiangzhang linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway
AT penggao linc00707regulatesautophagyandpromotestheprogressionoftriplenegativebreastcancerbyactivationofpi3kaktmtorpathway