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

Cell Death Discov

Department of Pathology, Qi Lu Hospital and School of Basic Medical Sciences, Shandong University, Shandong, China.

Published: March 2024

AI Article Synopsis

  • Triple-negative breast cancer (TNBC) is a highly aggressive subtype of breast cancer with a poor outlook, and the long non-coding RNA (LncRNA) Linc00707 has been found to be significantly elevated in TNBC tissues compared to normal and other breast cancer types.
  • Linc00707 enhances TNBC cell growth, migration, and invasion while influencing autophagy through the PI3K/AKT/mTOR signaling pathway.
  • Mechanistically, Linc00707 binds to miR-423-5p, increasing MARCH2 expression and promoting TNBC progression, suggesting its potential as a therapeutic target for patients with TNBC.

Article 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10940671PMC
http://dx.doi.org/10.1038/s41420-024-01906-7DOI Listing

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