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

被引:10
作者
Li, Hongli [1 ,2 ,3 ]
Liu, Qinghua [3 ]
Hu, Yaqiong [3 ]
Yin, Chonggao [4 ]
Zhang, Yunxiang [1 ,2 ,5 ]
Gao, Peng [1 ,2 ]
机构
[1] Shandong Univ, Qi Lu Hosp, Dept Pathol, Shandong, Peoples R China
[2] Shandong Univ, Sch Basic Med Sci, Shandong, Peoples R China
[3] Shandong Second Med Univ, Med Res Ctr, Shandong, Peoples R China
[4] Shandong Second Med Univ, Coll Nursing, Shandong, Peoples R China
[5] Shandong Second Med Univ, Weifang Peoples Hosp, Dept Pathol, Affiliated Hosp 1, Shandong, Peoples R China
基金
中国国家自然科学基金;
关键词
CELL-PROLIFERATION; MIGRATION; INVASION;
D O I
10.1038/s41420-024-01906-7
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页数:14
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