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

Hongli Li; Qinghua Liu; Yaqiong Hu; Chonggao Yin; Yunxiang Zhang; Peng Gao

doi:10.1038/s41420-024-01906-7

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

Cell Death Discov. 2024 Mar 14;10(1):138. doi: 10.1038/s41420-024-01906-7.

Authors

Hongli Li^{1

2}, Qinghua Liu², Yaqiong Hu², Chonggao Yin³, Yunxiang Zhang^#^{4

5}, Peng Gao^#⁶

Affiliations

¹ Department of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong University, Shandong, China.
² Medicine Research Center, Shandong Second Medical University, Shandong, China.
³ College of Nursing, Shandong Second Medical University, Shandong, China.
⁴ Department of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong University, Shandong, China. zhangbing199592@163.com.
⁵ Department of Pathology, First Affiliated Hospital of Shandong Second Medical University (Weifang People's Hospital), Shandong, China. zhangbing199592@163.com.
⁶ Department of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong University, Shandong, China. gaopeng@sdu.edu.cn.

^# Contributed equally.

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.